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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.
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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. What lymph node drains the sigmoid colon?
Inferior mesenteric
Fc
Interferon gamma; Th1
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

2. 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)?
TNF alpha and IL1
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
Hemochromatosis

3. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Not thymus - BM
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
Activates cytotoxic CD 8 T cells as second signal
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

4. What are the two signals required for B cell class switching? Which is the second signal?
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Hereditary angioedema; PNH
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

5. Which disease is associated with DR7?
Hereditary angioedema; PNH
Steroid responsive nephrotic syndrome
Immunosuppression after kidney transplantation
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

6. What lymph node drains the upper limb?
2 heavy chains and two light chains
Carbohydrate
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
Axillary

7. describe the pathogenesis of delayed type IV hypersensitivity
Activate macrophages
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)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

8. What is an example of a parasite showing antigenic variation?
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!
Antidote for digoxin intoxication
Secretory component
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

9. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Cytokine IL 10 secreted by Th2
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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

10. what prevents NK cells from killing normal cells if their default is to kill?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
MHC class molecules bind to KIRS or CD94 to prevent killing
Antimicrosomal and antithyroglobulin
IgG

11. where do somatic hypermutation and class switching occur?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
In the germinal center of secondary follicles (In the paler center)

12. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
IgM and IgG
Glycoproteins; HLA
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 :(
IgE; by activating eosinophils

13. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Inferior mesenteric
Anemias (esp due to renal failure)
CRP - C3b - IgM
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

14. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

15. What are the autoantibodies for type I diabetes mellitus?
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
Anti glutamate carboxylase and anti insulin
pentamer
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

16. Type IV hypersensitivity is i...
Inferior mesenteric
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
not Ab mediated
IgM and IgA

17. What is recomb alpha interferon used for?
Delayed type hypersensitivity
Anti SS- A (anti RO) and Anti SS- B
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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

18. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
...
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
A chemotactic factor for neutrophils

19. What are target cells?
Negative selection
isotype
Cells that stil have weird parts of their membrane that macrophages usually bite off
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

20. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
...
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

21. What does IL 4 do?
Interferon gamma; Th1
Cytokine IL 10 secreted by Th2
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
Acts as second signal on B cells to induce class switching to IgE and IgG

22. What is chronic mucocutaneous candidiasis d/t?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Pernicious Anemia and Hashimotos
Glycoproteins; HLA
T cell dysfunction

23. What are the three types of lymphocytes?
False! B cell class switching requires a second signal
Celiac
In the germinal center of secondary follicles (In the paler center)
B - T - and NK cells

24. What are the T cell functions?
Bind FcG for antibody dependent cellular cytotoxicity
Cells that stil have weird parts of their membrane that macrophages usually bite off
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

25. From where do cytokines come from?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Lymphocytes
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

26. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

27. What links the adaptive and innate immunity?
acute phase reactants
Complement activation (active in both)
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
Paracortex

28. What is filgrastim and sargramostim? and What is it used for?
Humoral
TLR ad nuclear receptors
Superficial inguinal
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

29. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Superior mesenteric
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
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

30. What are the labs in brutons agammaglobulinemia?
The igA found in breast milk
Not thymus - BM
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cross link

31. What is the main function of IL 8?
A chemotactic factor for neutrophils
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Fab portion

32. The lymphocytes are ________ origin
False! B cell class switching requires a second signal
mesenchymal
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

33. How is the thymus organized? what happens in each section?
T cell precursor
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti IF
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea

34. what cell surface marker is used for NK cells as it is unique to them?
CD56
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular 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
IgE

35. What is epo used for?
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
Lymphocytes
Anemias (esp due to renal failure)
Anti topoisomerase

36. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgG

37. What are the major functions of Antibodies?
Anti IF
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

38. What is digoxin immune Fab used for?
Basophils! THey want IG E class switch!
Viral neutralization of igM and IgG!
Anti IF
Antidote for digoxin intoxication

39. What lymph node drains the thigh?
Superficial inguinal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
No because no peptide fragment!
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

40. 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
Anemias (esp due to renal failure)
mesenchymal
Immunosuppression after kidney transplantation

41. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Fab portion
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgG

42. Describe the capsular structure of a lymph node; What are the functions of the LN?
Basophils! THey want IG E class switch!
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

43. What are C1 - C2 - C3 - C4 important for?
Its a serine protease that activates apoptosis; NK and CD8
The patient could become cyanotic in the OR!
Viral neutralization of igM and IgG!
Previous transfusion; pregnant woman whose fetus had paternal antigens

44. Which is the main antibody that provides passive immunity to infants?
Hemochromatosis
MS - hay fever - SLE - goodpastures
IgG
Its main effect is a defect in Ab opsonization for killing

45. Which type of selection of thymic development provides central tolerance?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Anemias (esp due to renal failure)
Negative selection

46. What is the pathogenesis of a candida skin test?
Chronic granulomatous disease
IL 15; IL 12 - interferon Beta and interferon alpha
Anti TSh receptor
Delayed type hypersensitivity

47. Which diseases are associated with DR2?
acute phase reactants
MS - hay fever - SLE - goodpastures
In the germinal center of secondary follicles (In the paler center)
IL 1 and IL 6

48. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Anti glutamate carboxylase and anti insulin
Antidesmoglein
Superior mesenteric
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

49. 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
IgE; by activating eosinophils
T cell precursor
Delayed type hypersensitivity

50. Monomer in circulation - ___ when secreted
Activates cytotoxic CD 8 T cells as second signal
Immunosuppression after kidney transplantation
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
dimer