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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. which antibody activate mast cells - basophils - and eosinophils?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IgE
Not thymus - BM

2. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
pale central germinal centers
DM type I and RA
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

3. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

4. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Thrombocytopenia
C5a
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

5. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Rheumatic arthritis
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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

6. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Para aortic
Bind FcG for antibody dependent cellular cytotoxicity
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

7. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Alternative splicing of mRNA
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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

8. which cells have more complete tolerance - B or T cells?
not Ab mediated
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
T
Internal iliac

9. which interleukin receptor is required for NK development? activation?
delayed!
opsonizes
Carbohydrate
IL 15; IL 12 - interferon Beta and interferon alpha

10. In thymic development - What is the positive selection? negative selections?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
...
MHC class molecules bind to KIRS or CD94 to prevent killing
When you select for which MHC it will have; take out the lymphs that self react

11. What is muromonab - CD3 (OKT3)
...
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
...
Edema and necrosis in that region

12. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
MHC I; from RER with help of the B2 microglobulin
The igA found in breast milk

13. How do you test for chronic granulomatous disease?
lowest concentration
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Negative nitroblue tetrazolium reduction test
DM type I

14. What does IgA pick up from epithelial cells before being secreted?
Secretory component
T cell precursor
Barrel hoop basement membrane fenestrations
Acts as second signal on B cells to induce class switching to IgE and IgG

15. What lymph node drains the anal canal (below the pectinate line)?
Paracortex
Superficial inguinal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
DM type I

16. What is the mechanism for sirolimus? what else it known as?
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
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

17. What do mature naive B lymphocytes express?
Yes
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IgM and IgD
Fab portion

18. Describe the capsular structure of a lymph node; What are the functions of the LN?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

19. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
Remove encapsulated bacateria
Secretory component
IL 5

20. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Inferior mesenteric
Previous transfusion; pregnant woman whose fetus had paternal antigens
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

21. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
When you select for which MHC it will have; take out the lymphs that self react
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

22. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Cytokine IL 10 secreted by Th2
MS
Paracortex
Anti Jo -1

23. Which MHC presents intracellular peptides? how so?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Liver! (they are proteins circulating in the blood)
Negative selection
MHC I; from RER with help of the B2 microglobulin

24. How does complement link innate and adaptive?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Acts as second signal on B cells to induce class switching to IgE and IgG
Local infection/inflammation; infection of the ln itself; metastasis
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

25. where do somatic hypermutation and class switching occur?
Immunosuppression after kidney transplantation
Antidesmoglein
type four
In the germinal center of secondary follicles (In the paler center)

26. which type of immunity is slow but long lasting? as opposed to...
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Interferon gamma; Th1
A j chain
Active; passive - fast but short half life (3 weeks!)

27. What are some catalase positive organisms?
Th cells fail to produce interferon gamma; a lot of IgE
S. aureus - E. Coli - aspergillus
MHC I - CD16 - CD56
Th2; Th1

28. What are the autoantibodies for type I diabetes mellitus?
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
Anti SS- A (anti RO) and Anti SS- B
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti glutamate carboxylase and anti insulin

29. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
A j chain
CRP - C3b - IgM

30. Name 5 ways Antibody diversity is generated?
secondary
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
pathogenesis
Th2; Th1

31. What are C1 - C2 - C3 - C4 important for?
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Viral neutralization of igM and IgG!
Hemochromatosis

32. What are the main symptoms of B cell immunodeficiencies?
Superficial inguinal
SP infections
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

33. what results in symptoms of shock in an acute hemolytic transfusion reaction?
DM type I and RA
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Activates Th1 helper cells; Macrophages

34. what characterizes an arthus reaction?
Anti topoisomerase
RNA segment reassortment
IgG
Edema and necrosis in that region

35. What is the pathogenesis of HyperIgE syndrome? What are the labs?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Th cells fail to produce interferon gamma; a lot of IgE
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
neutrophilia!

36. when can graft versus host disease? What is the result?
MS - hay fever - SLE - goodpastures
IgM and IgA
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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

37. What do multimeric antibodies require for assembly?
MS
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
A j chain
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

38. So antibodies are the effectors for the humoral response. List some of their functions.
neutrophilia!
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
A chemotactic factor for neutrophils
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

39. What bugs can actually infect the lymph node itself?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
CD21 on B cells (although there is T cell lymphocytosis in EBV)
2 heavy chains and two light chains

40. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
except hyperacute
CRP - C3b - IgM
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

41. To what portion of the Antibody do the complements bind?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Fc
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

42. How does the alternative pathway lead to MAC activation?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgE
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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

43. The two heavy chains of an antibody contribute to the...
Fab portion
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgAs in mothers breast milk!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

44. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
CRP - C3b - IgM
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anemias (esp due to renal failure)

45. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
The patient could become cyanotic in the OR!
Daclizumab; prevent ACUTE rejection of renal transplant
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgAs in mothers breast milk!

46. What are the autoantibodies for graves?
Anti viral and anti tumor
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti TSh receptor
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

47. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
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
IL 4
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

48. What are the autoantibodies for polymyositis and dermatomyositis?
Type IV
IgM and IgG
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti Jo -1

49. What type of side chains are found on Fc region of an antibody?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Carbohydrate
Interferon gamma; Th1

50. Which diseases are associated with DR2?
Daclizumab; prevent ACUTE rejection of renal transplant
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Fc
MS - hay fever - SLE - goodpastures