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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. which antibody is involved in the primary response or immediate response to an antigen?
IgM
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Antidote for digoxin intoxication
IgAs in mothers breast milk!

2. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Cytokine IL 10 secreted by Th2
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Glycoproteins; HLA

3. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
A chemotactic factor for neutrophils
cannot cross placenta
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

4. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
Thrombocytopenia
IL 1 and IL 6

5. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
MHC class molecules bind to KIRS or CD94 to prevent killing
Tetanus - Botulinum - HBV - Rabies
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

6. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Axillary
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

7. what bacteria are a splenectomy patient most susceptible to? why?
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
T cell dysfunction
Anti SS- A (anti RO) and Anti SS- B
A recomb cytokine of IL 2; RCC and metastatic melanoma

8. What is the clinical use of Muromonab?
Steroid responsive nephrotic syndrome
Severe pyogenic infections early in life
Immunosuppression after kidney transplantation
Activate macrophages

9. are Th cells involved in trapping of antigens of endotoxin/LPS?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
RNA segment reassortment
Its main effect is a defect in Ab opsonization for killing
No because no peptide fragment!

10. What is the presentation of hyperIgM syndrome?
delayed!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Previous transfusion; pregnant woman whose fetus had paternal antigens
Severe pyogenic infections early in life

11. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
MHC class molecules bind to KIRS or CD94 to prevent killing
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

12. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
In the germinal center of secondary follicles (In the paler center)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
By transcytosis

13. Which diseases are associated with DR4?
DM type I and RA
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

14. What lymph node drains the upper limb?
RNA segment reassortment
Axillary
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

15. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
DM type I
heavy chains
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

16. What is the white pulp of the spleen?
A - B - C; all the D's
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti IF
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

17. what cytokine does basophils secrete?
TNF alpha and IL1
IL 4
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
...

18. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
IgM and IgA
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

19. What is thrombopoietin used for?
Thrombocytopenia
Basophils! THey want IG E class switch!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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

20. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Cells that stil have weird parts of their membrane that macrophages usually bite off
Interferon gamma and IL 2
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

21. What are the autoantibodies for pemphigus bulgaris?
Anti TSh receptor
Antidesmoglein
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
secondary

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

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23. What is the pathology seen in chronic transplant rejection?
By transcytosis
Th cells fail to produce interferon gamma; a lot of IgE
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

24. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Activates Th1 helper cells; Macrophages
S. aureus - E. Coli - aspergillus
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

25. What lymph node drains the rectum (above the pectinate line)?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
not Ab mediated
Internal iliac

26. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Acts as second signal on B cells to induce class switching to IgE and IgG
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Interferon gamma and IL 2
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

27. IgM can exist as a _______ also
pentamer
Humoral
IgAs in mothers breast milk!
except hyperacute

28. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
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 :(
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Daclizumab; prevent ACUTE rejection of renal transplant
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

29. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

30. 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).
CD21 on B cells (although there is T cell lymphocytosis in EBV)
...
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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!

31. What are the autoantibodies for myasthenia gravis?
IgG
DM type I
Anti Ach receptor
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

32. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

33. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
MHC I; from RER with help of the B2 microglobulin
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Receiving preformed Antibodies
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

34. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
In the germinal center of secondary follicles (In the paler center)
Immunoflourescent staining of tissue biopsies
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

35. in which immunodef order do you see a lot of pus? no pus?
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Chronic granulomatous disease

36. Monomer in circulation - ___ when secreted
Rheumatic arthritis
dimer
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IgG

37. give an example of how influenza does a major antigenic shift.
NK cells
RNA segment reassortment
In the germinal center of secondary follicles (In the paler center)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

38. is IgM an opsonizer?
MS - hay fever - SLE - goodpastures
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Negative!

39. What are the autoantibodies for pernicious anemia?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
False! B cell class switching requires a second signal
Anti IF
SP infections

40. What is the pathology of acute transplant rejection? is it reversible?
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
Popliteal
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

41. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
except hyperacute
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

42. The lymphocytes are ________ origin
Activates cytotoxic CD 8 T cells as second signal
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
mesenchymal

43. The two heavy chains of an antibody contribute to the...
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Paracortex
Fab portion
neutrophilia!

44. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IgAs in mothers breast milk!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

45. Type IV hypersensitivity is i...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Negative!
isotype
not Ab mediated

46. What are the main Cell surface proteins on T cells?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
T cell dysfunction
Antidote for digoxin intoxication
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

47. 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?
cannot cross placenta
Graves
Previous transfusion; pregnant woman whose fetus had paternal antigens
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. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Th cells fail to produce interferon gamma; a lot of IgE
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Remove encapsulated bacateria

49. What type of side chains are found on Fc region of an antibody?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Carbohydrate

50. What is the marginal zone of the spleen? what happens there?
except hyperacute
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

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USMLE Step 1 Immunology

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