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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 lymph node drains the stomach?
In the germinal center of secondary follicles (In the paler center)
SP infections
Celiac
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

2. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Yes
IgE
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

3. What type of fenestrations are found in the red pulp of the spleen?
Influenza; antigenic shift; antigenic drift
RNA segment reassortment
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Barrel hoop basement membrane fenestrations

4. Name 5 ways Antibody diversity is generated?
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
heavy chains
Antimicrosomal and antithyroglobulin
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

5. What lymph node drains the scrotum?
NK cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
Superficial inguinal
Anti IF

6. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
MS
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Increases expression of MHC I and MHC II and also activates NK cells
Paracortex

7. What is a factor that is a predictor for a bad transplantation?
IgM
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
Popliteal

8. 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
Acts as second signal on B cells to induce class switching to IgE and IgG
A - B - C; all the D's
Activates Th1 helper cells; Macrophages

9. What is the common variable immunodeficiency ? How is it different from Brutons?
In the germinal center of secondary follicles (In the paler center)
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
All MHC 1/CD8
...

10. What is filgrastim and sargramostim? and What is it used for?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Antidote for digoxin intoxication
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Not thymus - BM

11. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Severe pyogenic infections early in life
TNF alpha and IL1
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

12. when can graft versus host disease? What is the result?
CD56
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
A j chain
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

13. How does complement link innate and adaptive?
Negative selection
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
False! B cell class switching requires a second signal
Cells that stil have weird parts of their membrane that macrophages usually bite off

14. What is recomb beta interferon used for?
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
Recom IL 11; thrombocytopenia
MS
dimer

15. So antibodies are the effectors for the humoral response. List some of their functions.
Macrophages - Dendritic cells - B cells
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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 antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

16. Describe complement dependent Type II hypersensitivity. Give an example.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
T

17. The pathogenesis of contact dermatitis is ________ hypersensitivity
isotype
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
type four

18. How fast does it occur?
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
The patient could become cyanotic in the OR!
Steroid responsive nephrotic syndrome
Macrophages - Dendritic cells - B cells

19. Which is the most abundant antibody in blood?
IgG
cannot cross placenta
Antimicrosomal and antithyroglobulin
delayed!

20. What does IgA pick up from epithelial cells before being secreted?
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
False! B cell class switching requires a second signal
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
Secretory component

21. What is the main function of interferons?
...
Active; passive - fast but short half life (3 weeks!)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

22. What are the autoantibodies for systemic sclerosis?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Anti topoisomerase

23. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

24. What does granulysin do?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

25. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
No because no peptide fragment!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Anti glutamate carboxylase and anti insulin

26. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Anti topoisomerase
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

27. What are MHC's necessary for? By themselves?
MHC II - B7
Para aortic
delayed!
T cell activation; no with CD 4 or CD 8

28. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
When you select for which MHC it will have; take out the lymphs that self react
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
...

29. How does igA cross the epithelium?
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
By transcytosis
Anti U1 RNP (ribonucleoprotein)
opsonizes

30. What kinds of receptors activate innate immunity?
Antihistone
Immunoflourescent staining of tissue biopsies
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
TLR ad nuclear receptors

31. What are the autoantibodies for primary biliary cirrhosis?
Cross link
Anti TSh receptor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti mitochondrial

32. What is passive immunity?
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Receiving preformed Antibodies
IgG

33. What happens in a deficiency of C3?
Th2; Th1
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

34. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
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

35. What is the pathogenesis of a candida skin test?
MHC I; from RER with help of the B2 microglobulin
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)
Delayed type hypersensitivity
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

36. Which are the only two antiinflammatory cytokines?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
TGF beta and IL 10

37. Which helper T cells' development is induced by IL 4? IL 12?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Its main effect is a defect in Ab opsonization for killing
Th2; Th1
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

38. what ensure that a memory response is generated?
IgM and IgG
If there is class switching and plasma cell production (that is when memory cells are produced)
...
Anti TSh receptor

39. What is the general structure of an Ab?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Anemias (esp due to renal failure)
2 heavy chains and two light chains
S. aureus - E. Coli - aspergillus

40. Which antibodies can be multimeric?
IgM and IgA
Glycoproteins; HLA
opsonizes
Type IV

41. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Its main effect is a defect in Ab opsonization for killing
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

42. What is the pathology seen in chronic transplant rejection?
cannot cross placenta
False! B cell class switching requires a second signal
...
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

43. Describe the capsular structure of a lymph node; What are the functions of the LN?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Acts as second signal on B cells to induce class switching to IgE and IgG

44. What are the cell surface proteins on NK cells?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
MHC I - CD16 - CD56
Anti smooth muscle
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

45. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
...
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

46. What do mature naive B lymphocytes express?
IgM and IgD
mesenchymal
heavy chains
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

47. What are the main symptoms of B cell immunodeficiencies?
Chronic granulomatous disease
SP infections
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (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

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

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49. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

50. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
pale central germinal centers
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
Paracortex; viral infection