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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Alternative splicing of mRNA

2. Which disease is associated with B8?
Graves
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
pale central germinal centers

3. Which is the main antibody that provides passive immunity to infants?
IgG
pathogenesis
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

4. when can graft versus host disease? What is the result?
Popliteal
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
T cell dysfunction
except hyperacute

5. Which disease is associated with DR7?
Negative nitroblue tetrazolium reduction test
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
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
Steroid responsive nephrotic syndrome

6. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Hereditary angioedema; PNH
secondary
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

7. What is the main function of IL 8?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Interferon gamma; Th1
A chemotactic factor for neutrophils

8. Which diseases are associated with DR4?
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IL 3; supports growth and differentiation of bone marrow stem cells
DM type I and RA

9. What is hereditary angioedema? What are the C3 levels?
Local infection/inflammation; infection of the ln itself; metastasis
The igA found in breast milk
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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

10. A lymph node is a ________ lymphoid organ.
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Antibody mediated cytotoxicity; either complement dependent or complement independent
secondary
Activate macrophages

11. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
MS
Axillary
Th cells fail to produce interferon gamma; a lot of IgE

12. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Secretory component
IL 4 - 5 - 10 - 6
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
except hyperacute

13. What is serum sickness? give an example.
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Superficial inguinal
Influenza; antigenic shift; antigenic drift
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

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

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15. The secondary follicles have __________; primary follicles are dense
Interferon gamma; Th1
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
pale central germinal centers
Cytokine IL 10 secreted by Th2

16. 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
Immunosuppression after kidney transplantation
In the germinal center of secondary follicles (In the paler center)
Cells that stil have weird parts of their membrane that macrophages usually bite off

17. What is the presentation of Brutons agammaglobulinemia?
2 heavy chains and two light chains
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

18. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

19. Monomer in circulation - ___ when secreted
dimer
...
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Antimicrosomal and antithyroglobulin

20. which of the hypersensitivity reactions is not Ab mediated?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Cross link
The igA found in breast milk
Type IV

21. What is the main cytokine released by T cells? What does it do
IL 4 - 5 - 10 - 6
Local infection/inflammation; infection of the ln itself; metastasis
IL 3; supports growth and differentiation of bone marrow stem cells
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

22. __________ are a part of the innate system.
Lymphocytes
NK cells
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgM and IgG

23. 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).
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!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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 :(

24. what characterizes an arthus reaction?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Edema and necrosis in that region
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

25. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
CD56
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
heavy chains

26. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
encapsulated
Daclizumab; prevent ACUTE rejection of renal transplant
neutrophilia!
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

27. The pathogenesis of contact dermatitis is ________ hypersensitivity
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Fab portion
Viral neutralization of igM and IgG!
type four

28. What are the autoantibodies for graves?
Anti TSh receptor
Chronic granulomatous disease
No because no peptide fragment!
Axillary

29. What does granzyme do? who secretes it?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
opsonizes
Its a serine protease that activates apoptosis; NK and CD8
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

30. 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
Superficial inguinal
Immunosuppression after kidney transplantation
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

31. What is thrombopoietin used for?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
isotype
Thrombocytopenia
Popliteal

32. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Barrel hoop basement membrane fenestrations

33. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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

34. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
carboxy terminal
Wiskott Aldrich syndrome

35. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
Cross link
mesenchymal
Yes

36. Describe the Mannose Lectin pathway
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
opsonizes
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

37. Describe the capsular structure of a lymph node; What are the functions of the LN?
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
In the germinal center of secondary follicles (In the paler center)
S. aureus - E. Coli - aspergillus
Glycoproteins; HLA

38. Name the three opsonins
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
S. aureus - E. Coli - aspergillus
Negative selection
CRP - C3b - IgM

39. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
False! B cell class switching requires a second signal
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

40. What cytokines are released by Th1 cells?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Previous transfusion; pregnant woman whose fetus had paternal antigens
Interferon gamma and IL 2
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

41. What does it mean if there are igM in the serum at birth?
Superficial inguinal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Fc
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

42. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Antihistone
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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

43. What are the autoantibodies for Mixed connective tissue disease?
...
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Negative nitroblue tetrazolium reduction test
Anti U1 RNP (ribonucleoprotein)

44. How fast does it occur?
The patient could become cyanotic in the OR!
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
IgE
DM type I and RA

45. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Delayed type hypersensitivity
...
Hemochromatosis

46. How does the alternative pathway lead to MAC activation?
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
SP infections
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)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

47. What is the marginal zone of the spleen? what happens there?
Secretory component
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

48. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
delayed!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Thrombocytopenia

49. What is anergy? why does this occur?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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

50. Which cytokines do Th2 release and For what?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

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USMLE Step 1 Immunology

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