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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. Type IV hypersensitivity is i...
...
not Ab mediated
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

2. What does interferon gamma do? What two type of cells does it attack mostly?
TNF alpha and IL1
Pernicious Anemia and Hashimotos
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
opsonizes

3. What is the toxicity of azathioprine?
2 heavy chains and two light chains
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
...
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

4. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

5. What is three common causes of severe combined immunodef? What is the result of all three?
Popliteal
IgG
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

6. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Superior mesenteric
Anti mitochondrial
Rheumatic arthritis
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

7. What are some sinopulmonary infections?
Daclizumab; prevent ACUTE rejection of renal transplant
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Sinusitis - otitis media - pneumonia
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

8. In thymic development - What is the positive selection? negative selections?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
DM type I
When you select for which MHC it will have; take out the lymphs that self react

9. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Glycoproteins; HLA

10. which interleukin receptor is required for NK development? activation?
IgAs in mothers breast milk!
MHC II - B7
Delayed type hypersensitivity
IL 15; IL 12 - interferon Beta and interferon alpha

11. What is the presentation of common variable immunodef? and What are the labs?
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
Severe pyogenic infections early in life
Receiving preformed Antibodies
RNA segment reassortment

12. what prevents NK cells from killing normal cells if their default is to kill?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
T cell activation; no with CD 4 or CD 8
MHC class molecules bind to KIRS or CD94 to prevent killing
Viral neutralization of igM and IgG!

13. What are the two signals required for B cell class switching? Which is the second signal?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IgM and IgD
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgE

14. What are the autoantibodies for primary biliary cirrhosis?
Kill them because they have CD16 on them that recognize the FcG portion
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Yes
Anti mitochondrial

15. What are the autoantibodies for pemphigus bulgaris?
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antidesmoglein

16. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Anti TSh receptor
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Hereditary angioedema; PNH
Histamine; post capillary venules - vasodilation

17. hat is the presentation of Jobs syndrome or Hyper IgE?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Internal iliac
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

18. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Anti mitochondrial
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
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

19. Which are the only two antiinflammatory cytokines?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
TGF beta and IL 10
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Humoral

20. Give an example of someone who could get hyperacute transplant rejection.
Anti U1 RNP (ribonucleoprotein)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Previous transfusion; pregnant woman whose fetus had paternal antigens

21. What lymph node drains the rectum (above the pectinate line)?
opsonizes
Influenza; antigenic shift; antigenic drift
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
Internal iliac

22. How does igA cross the epithelium?
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
By transcytosis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Axillary

23. What is the pathogenesis of a hypersensitivity reaction?
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Acts as second signal on B cells to induce class switching to IgE and IgG

24. What is colostrum?
Anti Ach receptor
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
The igA found in breast milk
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

25. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
No because no peptide fragment!
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

26. What is Aldesleukin? What is it used for
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
A recomb cytokine of IL 2; RCC and metastatic melanoma
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

27. How is sirolimus different from tacrolimus?
TNF alpha and IL1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
secondary
Paracortex

28. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Anti smooth muscle
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Remove encapsulated bacateria

29. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
IL 15; IL 12 - interferon Beta and interferon alpha
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

30. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
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
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

31. which cells have more complete tolerance - B or T cells?
IgM and IgA
T
Rheumatic arthritis
Basophils! THey want IG E class switch!

32. 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
The patient could become cyanotic in the OR!
MHC I - CD16 - CD56
Hemochromatosis

33. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Its a serine protease that activates apoptosis; NK and CD8
IgG
Negative selection

34. What is the main function of interferons?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Graves
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

35. What does granulysin do?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MS
The igA found in breast milk
NK cells

36. other than C3a - what other complement acts as an anaphyloxin?
Influenza; antigenic shift; antigenic drift
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
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
C5a

37. when can graft versus host disease? What is the result?
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
IgG
Graves
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

38. What are target cells?
Rheumatic arthritis
...
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

39. What lymph node drains the anal canal (below the pectinate line)?
IgE; by activating eosinophils
Superficial inguinal
dimer
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

40. What links the adaptive and innate immunity?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgE; by activating eosinophils
Complement activation (active in both)
All MHC 1/CD8

41. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
The patient could become cyanotic in the OR!
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 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 :(

42. What does IgA pick up from epithelial cells before being secreted?
Celiac
Secretory component
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

43. Only the _______ contribute to the Fc region
heavy chains
Th cells fail to produce interferon gamma; a lot of IgE
Humoral
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

44. are Th cells involved in trapping of antigens of endotoxin/LPS?
type four
No because no peptide fragment!
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
Antimicrosomal and antithyroglobulin

45. What lymph node drains the upper limb?
Axillary
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
Superior mesenteric
MHC I; from RER with help of the B2 microglobulin

46. To what portion of the Antibody do the complements bind?
MHC class molecules bind to KIRS or CD94 to prevent killing
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Fc
Increases expression of MHC I and MHC II and also activates NK cells

47. What are the main symptoms of B cell immunodeficiencies?
IL 1 and IL 6
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
SP infections

48. What do mature naive B lymphocytes express?
IgM and IgD
IgG
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

49. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
...
acute phase reactants
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

50. What is the cause of thymic aplasia? What is its presentation? What are the labs?
neutrophilia!
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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 SS- A (anti RO) and Anti SS- B