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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 interleukin receptor is required for NK development? activation?
Anti Ach receptor
Fab portion
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)
IL 15; IL 12 - interferon Beta and interferon alpha

2. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Immunosuppression after kidney transplantation
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

3. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Basophils! THey want IG E class switch!
Antibody mediated cytotoxicity; either complement dependent or complement independent
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

4. What are the autoantibodies for autoimmune hepatitis?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti smooth muscle
Superficial inguinal
Celiac

5. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Its a serine protease that activates apoptosis; NK and CD8
Daclizumab; prevent ACUTE rejection of renal transplant
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

6. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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)
A j chain

7. what will NK cells do to cells covered in IgG Ab? why?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Kill them because they have CD16 on them that recognize the FcG portion

8. What is the defect in hyper IgM syndrome? What are the lab results?
acute phase reactants
The patient could become cyanotic in the OR!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

9. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Local infection/inflammation; infection of the ln itself; metastasis
Activates Th1 helper cells; Macrophages
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

10. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
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
Hereditary angioedema; PNH
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

11. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a 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
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

12. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IL 1 and IL 6
C5a
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

13. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
mesenchymal

14. in which immunodef order do you see a lot of pus? no pus?
Superior mesenteric
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Bind FcG for antibody dependent cellular cytotoxicity
Negative selection

15. what happens in a deficiency of C1 esterase inhibitor? DAF?
Superior mesenteric
Acts as second signal on B cells to induce class switching to IgE and IgG
Hereditary angioedema; PNH
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

16. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti alpha subunit 3 of collagen on type IV bm
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

17. How does igA cross the epithelium?
C5a
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
By transcytosis

18. where do NK cells develop?
Not thymus - BM
False! B cell class switching requires a second signal
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgM and IgG

19. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Anti glutamate carboxylase and anti insulin
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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

20. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
By transcytosis
IgM and IgG
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

21. What does IL 10 do? who is secreted by?
MS
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

22. Describe the capsular structure of a lymph node; What are the functions of the LN?
NK cells
Cyclosporine - OKT3
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
Paracortex; viral infection

23. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Anti topoisomerase
acute phase reactants
When you select for which MHC it will have; take out the lymphs that self react
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

24. What are the autoantibodies for myasthenia gravis?
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 Ach receptor
opsonizes
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

25. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Steroid responsive nephrotic syndrome
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
By transcytosis

26. What is passive immunity?
Steroid responsive nephrotic syndrome
secondary
Anti SS- A (anti RO) and Anti SS- B
Receiving preformed Antibodies

27. Which disease is associated with HLA A3?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Hemochromatosis
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
isotype

28. IgG...
opsonizes
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Carbohydrate
Barrel hoop basement membrane fenestrations

29. What type of side chains are found on Fc region of an antibody?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Superficial inguinal
Carbohydrate
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

30. The idiotype; the Fc portion determines the...
IgM
Thrombocytopenia
isotype
Previous transfusion; pregnant woman whose fetus had paternal antigens

31. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Rheumatic arthritis
Cross link
Fab portion
...

32. which of the transplant rejections is antibody mediated? why does it occur?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
T cell dysfunction
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Popliteal

33. From where do cytokines come from?
IgG
IgG
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Lymphocytes

34. What are target cells?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Cells that stil have weird parts of their membrane that macrophages usually bite off
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
...

35. What are some sinopulmonary infections?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Sinusitis - otitis media - pneumonia
Cytokine IL 10 secreted by Th2
DM type I and RA

36. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
IgAs in mothers breast milk!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Tetanus - Botulinum - HBV - Rabies
Active; passive - fast but short half life (3 weeks!)

37. What is recomb alpha interferon used for?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

38. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
pathogenesis
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

39. What is the toxicity of azathioprine?
...
A chemotactic factor for neutrophils
IgG
Type IV

40. A lymph node is a ________ lymphoid organ.
T cell dysfunction
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
C5a
secondary

41. What is the general structure of an Ab?
2 heavy chains and two light chains
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Not thymus - BM

42. What lymph node drains the thigh?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Cross link
Superficial inguinal
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

43. What bugs can actually infect the lymph node itself?
IgM and IgA
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

44. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
MHC class molecules bind to KIRS or CD94 to prevent killing
Activates cytotoxic CD 8 T cells as second signal
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

45. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
DM type I and RA
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
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
Negative!

46. What are the major functions of Antibodies?
IgAs in mothers breast milk!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anemias (esp due to renal failure)

47. What is the mechanism for sirolimus? what else it known as?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
DM type I and RA
Anemias (esp due to renal failure)

48. Which is the most abundant antibody in blood?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgM and IgG
IgG
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

49. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Activates cytotoxic CD 8 T cells as second signal
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Anemias (esp due to renal failure)
CRP - C3b - IgM

50. What are C1 - C2 - C3 - C4 important for?
Secretory component
Edema and necrosis in that region
Viral neutralization of igM and IgG!
IgA