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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 results in symptoms of shock in an acute hemolytic transfusion reaction?
Type IV
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

2. What are the T cell functions?
Barrel hoop basement membrane fenestrations
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cells that stil have weird parts of their membrane that macrophages usually bite off
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

3. which antibodies prevent antigens from binding mucosal surfaces?
Interferon gamma; Th1
By transcytosis
A chemotactic factor for neutrophils
IgA

4. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Antibody mediated cytotoxicity; either complement dependent or complement independent
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Axillary
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

5. What are the cell surface proteins for Macrophages? which two are for opsonins?
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
Increases expression of MHC I and MHC II and also activates NK cells
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

6. What is recomb beta interferon used for?
MS
Pernicious Anemia and Hashimotos
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti alpha subunit 3 of collagen on type IV bm

7. in which immunodef order do you see a lot of pus? no pus?
Fab portion
Thrombocytopenia
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Kill them because they have CD16 on them that recognize the FcG portion

8. 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?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Superficial inguinal
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
IgG

9. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

10. Complements are...
TLR ad nuclear receptors
acute phase reactants
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

11. 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
Edema and necrosis in that region
Anti topoisomerase
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

12. describe the pathogenesis of delayed type IV hypersensitivity
Anti glutamate carboxylase and anti insulin
By transcytosis
Active; passive - fast but short half life (3 weeks!)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

13. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Negative!
MHC I - CD16 - CD56
pentamer

14. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
TNF alpha and IL1

15. Name 5 ways Antibody diversity is generated?
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
acute phase reactants
If there is class switching and plasma cell production (that is when memory cells are produced)
RNA segment reassortment

16. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Kill them because they have CD16 on them that recognize the FcG portion
Not thymus - BM
Fab portion

17. Which disease is associated with DR7?
Histamine; post capillary venules - vasodilation
Steroid responsive nephrotic syndrome
A chemotactic factor for neutrophils
Complement activation (active in both)

18. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

19. which B and T cell disorder presents with specifically low IgM?
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
Wiskott Aldrich syndrome
TLR ad nuclear receptors
except hyperacute

20. What is the main function of IL 8?
Para aortic
IL 5
Anti glutamate carboxylase and anti insulin
A chemotactic factor for neutrophils

21. hat is the presentation of Jobs syndrome or Hyper IgE?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IL 4 - 5 - 10 - 6
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti smooth muscle

22. What are the autoantibodies for other vasculitides?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
By transcytosis

23. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
secondary
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM
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

24. What is an example of a parasite showing antigenic variation?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Paracortex; viral infection
T cell activation; no with CD 4 or CD 8
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

25. What are howell jolly bodies?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
heavy chains
Thrombocytopenia
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

26. Which disease is associated with DR3?
Cytokine IL 10 secreted by Th2
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
A chemotactic factor for neutrophils
DM type I

27. What is the pathogenesis of a candida skin test?
Anti glutamate carboxylase and anti insulin
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
Delayed type hypersensitivity
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

28. What is a factor that is a predictor for a bad transplantation?
Superficial inguinal
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Cross link
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

29. What are superantigens? give two examples.
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
Anti topoisomerase
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

30. What is the presentation of Brutons agammaglobulinemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
If there is class switching and plasma cell production (that is when memory cells are produced)

31. What is the main cytokine that activates eosinophils?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Thrombocytopenia
IL 5
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

32. What is anergy? why does this occur?
Anti U1 RNP (ribonucleoprotein)
Liver! (they are proteins circulating in the blood)
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

33. Which diseases are associated with DR4?
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
Rheumatic arthritis
Superficial inguinal
DM type I and RA

34. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Anti Jo -1
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)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
carboxy terminal

35. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
Anti glutamate carboxylase and anti insulin
Macrophages - Dendritic cells - B cells

36. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

37. What are the cell surface proteins on NK cells?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
MHC I - CD16 - CD56
TLR ad nuclear receptors

38. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Antibody mediated cytotoxicity; either complement dependent or complement independent
B - T - and NK cells
Increases expression of MHC I and MHC II and also activates NK cells

39. What is passive immunity?
heavy chains
Receiving preformed Antibodies
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
carboxy terminal

40. What is the toxicity of azathioprine?
Anti Jo -1
TGF beta and IL 10
...
T cell precursor

41. What are the main symptoms of B cell immunodeficiencies?
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
SP infections
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

42. What are some sinopulmonary infections?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Sinusitis - otitis media - pneumonia
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

43. Which is the most abundant antibody in blood?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgG
Axillary
Fab portion

44. What are the autoantibodies for drug induced lupus?
Popliteal
Cells that stil have weird parts of their membrane that macrophages usually bite off
Antihistone
Tetanus - Botulinum - HBV - Rabies

45. What are MHC's necessary for? By themselves?
Sinusitis - otitis media - pneumonia
RNA segment reassortment
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
T cell activation; no with CD 4 or CD 8

46. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Secretory component
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

47. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
pentamer

48. What are the autoantibodies for pemphigus bulgaris?
Glycoproteins; HLA
RNA segment reassortment
Antidesmoglein
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

49. What lymph node drains the rectum (above the pectinate line)?
S. aureus - E. Coli - aspergillus
Internal iliac
Carbohydrate
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

50. To what portion of the Antibody do the complements bind?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgA
Fc
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma