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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 is the general structure of an Ab?
Activates cytotoxic CD 8 T cells as second signal
2 heavy chains and two light chains
TGF beta and IL 10
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

2. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Superior mesenteric
Anti viral and anti tumor

3. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Antimicrosomal and antithyroglobulin
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Popliteal
Anti Jo -1

4. What lymph node drains the testes?
Para aortic
Pernicious Anemia and Hashimotos
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

5. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
False! B cell class switching requires a second signal
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

6. What does IL 5 do?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
CD56
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

7. What are the two signals to kill for NK cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Influenza; antigenic shift; antigenic drift
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Antidesmoglein

8. A lymph node is a ________ lymphoid organ.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Antidesmoglein
secondary
Macrophages - Dendritic cells - B cells

9. what mediates the type II hypersensitivity? What are the two different methods?
Axillary
Histamine; post capillary venules - vasodilation
Antibody mediated cytotoxicity; either complement dependent or complement independent
...

10. 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
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 :(
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
In the germinal center of secondary follicles (In the paler center)

11. Which antibodies can be multimeric?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
If there is class switching and plasma cell production (that is when memory cells are produced)
IgM and IgA
Stimulate the liver to release acute phase reactants

12. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

13. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Chronic granulomatous disease
Acts as second signal on B cells to induce class switching to IgE and IgG
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

14. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
All MHC 1/CD8
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

15. What is immune complex disease? give an example.
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

16. What does IL 2 do?
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
Activates cytotoxic CD 8 T cells as second signal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

17. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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!
Daclizumab; prevent ACUTE rejection of renal transplant
Antibody mediated cytotoxicity; either complement dependent or complement independent

18. Only the _______ contribute to the Fc region
heavy chains
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Lymphocytes

19. what prevents NK cells from killing normal cells if their default is to kill?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti Ach receptor
MHC class molecules bind to KIRS or CD94 to prevent killing
Antidesmoglein

20. In general What are T cells good for?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti viral and anti tumor
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

21. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
IL 1 and IL 6
...
Influenza; antigenic shift; antigenic drift
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

22. give an example of how influenza does a major antigenic shift.
Sinusitis - otitis media - pneumonia
Fc
Paracortex; viral infection
RNA segment reassortment

23. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti mitochondrial
TLR ad nuclear receptors
Yes

24. What are the main symptoms of B cell immunodeficiencies?
Anti glutamate carboxylase and anti insulin
SP infections
Basophils! THey want IG E class switch!
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

25. What are the autoantibodies for goodpastures syndrome?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IgA
Anti SS- A (anti RO) and Anti SS- B
Anti alpha subunit 3 of collagen on type IV bm

26. 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
...
Viral neutralization of igM and IgG!
Popliteal

27. other than C3a - what other complement acts as an anaphyloxin?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
C5a
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Sinusitis - otitis media - pneumonia

28. What are the function of B cells?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

29. __________ are a part of the innate system.
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
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
NK cells
Secretory component

30. what characterizes an arthus reaction?
Increases expression of MHC I and MHC II and also activates NK cells
Thrombocytopenia
Edema and necrosis in that region
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

31. What lymph node drains the thigh?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Superficial inguinal
Fab portion

32. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
encapsulated
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

33. what cytokine does basophils secrete?
DM type I
...
IL 4
Lymphocytes

34. Describe the Mannose Lectin pathway
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
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
Interferon gamma; Th1
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

35. Which diseases are associated with DR2?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
pathogenesis
MS - hay fever - SLE - goodpastures
Paracortex

36. What is the receptor for EBV? On what cells is that located?
The patient could become cyanotic in the OR!
Anti smooth muscle
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antimicrosomal and antithyroglobulin

37. The lymphocytes are ________ origin
MHC I - CD16 - CD56
mesenchymal
Immunosuppression after kidney transplantation
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

38. What is three common causes of severe combined immunodef? What is the result of all three?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
CRP - C3b - IgM
Axillary

39. What is chronic mucocutaneous candidiasis d/t?
MS
Axillary
T cell dysfunction
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

40. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Chronic granulomatous disease
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgM and IgG

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

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42. What does interferon gamma do to be antiviral?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Negative nitroblue tetrazolium reduction test
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Increases expression of MHC I and MHC II and also activates NK cells

43. What are the autoantibodies for autoimmune hepatitis?
Type IV
Anti smooth muscle
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

44. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Basophils! THey want IG E class switch!
Histamine; post capillary venules - vasodilation
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

45. What lymph node drains the rectum (above the pectinate line)?
MHC I - CD16 - CD56
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Internal iliac

46. What is the clinical use for sirolimus? what should you combine it with?
Rheumatic arthritis
TNF alpha and IL1
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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

47. What is a factor that is a predictor for a bad transplantation?
Activate macrophages
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti Jo -1

48. What lymph node drains the sigmoid colon?
cannot cross placenta
delayed!
Severe pyogenic infections early in life
Inferior mesenteric

49. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Yes
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
T cell activation; no with CD 4 or CD 8
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!

50. 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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
secondary
Antihistone