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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. 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
When you select for which MHC it will have; take out the lymphs that self react
Yes
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

2. What is anergy? why does this occur?
Edema and necrosis in that region
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Kill them because they have CD16 on them that recognize the FcG portion
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

3. Which is the main antibody that provides passive immunity to infants?
IgG
IgAs in mothers breast milk!
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

4. What lymph node drains the stomach?
Celiac
MHC I; from RER with help of the B2 microglobulin
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Negative!

5. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

6. ________ regulate the cell mediated response.
Anti U1 RNP (ribonucleoprotein)
Chronic granulomatous disease
Humoral
pale central germinal centers

7. What are the three types of APCs?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Macrophages - Dendritic cells - B cells
Th2; Th1
Remove encapsulated bacateria

8. How do you test for chronic granulomatous disease?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Negative nitroblue tetrazolium reduction test
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
RNA segment reassortment

9. So antibodies are the effectors for the humoral response. List some of their functions.
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
2 heavy chains and two light chains
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

10. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antimicrosomal and antithyroglobulin
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

11. 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 class molecules bind to KIRS or CD94 to prevent killing
Anemias (esp due to renal failure)
IgM

12. What are target cells?
Its main effect is a defect in Ab opsonization for killing
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Cells that stil have weird parts of their membrane that macrophages usually bite off
DM type I

13. What is recomb gamma interferon used for?
Anti IF
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
Chronic granulomatous disease
All MHC 1/CD8

14. What is recomb beta interferon used for?
MS
Glycoproteins; HLA
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Activates cytotoxic CD 8 T cells as second signal

15. What is the pathogenesis of a hypersensitivity reaction?
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
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
secondary
Immunosuppression after kidney transplantation

16. other than eat and bite RBCs what else do Macrophages of spleen do>
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Remove encapsulated bacateria
Hemochromatosis

17. Which type of selection of thymic development provides central tolerance?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Anti SS- A (anti RO) and Anti SS- B
In the germinal center of secondary follicles (In the paler center)
Negative selection

18. What is the pathogenesis of acute transplant rejection? When does it occur?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
not Ab mediated
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

19. what cell surface marker is used for NK cells as it is unique to them?
CD56
False! B cell class switching requires a second signal
Edema and necrosis in that region
No because no peptide fragment!

20. What happens in a deficiency of C3?
Macrophages - Dendritic cells - B cells
Recom IL 11; thrombocytopenia
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
CD21 on B cells (although there is T cell lymphocytosis in EBV)

21. What is the general structure of an Ab?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IL 1 and IL 6
2 heavy chains and two light chains

22. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Remove encapsulated bacateria
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

23. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti glutamate carboxylase and anti insulin

24. what cell surface proteins are on all APCs?
MHC II - B7
carboxy terminal
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
CRP - C3b - IgM

25. What are some catalase positive organisms?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
S. aureus - E. Coli - aspergillus
Paracortex; viral infection

26. To what portion of the Antibody do the complements bind?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Fc
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
The patient could become cyanotic in the OR!

27. What are MHC's necessary for? By themselves?
MHC II - B7
T cell activation; no with CD 4 or CD 8
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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

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

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29. What are the main symptoms of T cell immunodeficiencies?
Inferior mesenteric
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

30. What is the most common example of passive immunity?
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
IgAs in mothers breast milk!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

31. The alternative pathway is the only constutively...
active complement pathway
Hereditary angioedema; PNH
B - T - and NK cells
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

32. What are the two signals required for Th1 cells? what happens after then activated?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Th cells fail to produce interferon gamma; a lot of IgE
Anti mitochondrial
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

33. what mediates the type II hypersensitivity? What are the two different methods?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antibody mediated cytotoxicity; either complement dependent or complement independent
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Viral neutralization of igM and IgG!

34. For which toxins are preformed antibodies (passive) given?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Tetanus - Botulinum - HBV - Rabies
TGF beta and IL 10

35. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
Anti viral and anti tumor
dimer

36. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
cannot cross placenta
delayed!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

37. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
not Ab mediated
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

38. which type of immunity is slow but long lasting? as opposed to...
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
Stimulate the liver to release acute phase reactants
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Active; passive - fast but short half life (3 weeks!)

39. is IgM an opsonizer?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Negative!
neutrophilia!

40. Type Iv hypersensitivity is...
delayed!
NK cells
Anti viral and anti tumor
IgM and IgA

41. Give three examples of bacteria that use antigenic variation and how.
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A - B - C; all the D's
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

42. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Humoral
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
NK cells

43. What lymph node drains the upper limb?
Influenza; antigenic shift; antigenic drift
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
type four
Axillary

44. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
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
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 :(
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

45. 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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Sinusitis - otitis media - pneumonia
Activates cytotoxic CD 8 T cells as second signal

46. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Secretory component
Chronic granulomatous disease
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

47. What are C1 - C2 - C3 - C4 important for?
not Ab mediated
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 15; IL 12 - interferon Beta and interferon alpha
Viral neutralization of igM and IgG!

48. What is the most common selective Ig deficiency? What is the presentation?
IgM
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

49. What are the autoantibodies for myasthenia gravis?
When you select for which MHC it will have; take out the lymphs that self react
except hyperacute
Superficial inguinal
Anti Ach receptor

50. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Cyclosporine - OKT3
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
The patient could become cyanotic in the OR!