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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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1. What is the main function of IL 8?
Cross link
IgM and IgG
A chemotactic factor for neutrophils
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

2. What is hereditary angioedema? What are the C3 levels?
...
TLR ad nuclear receptors
Cytokine IL 10 secreted by Th2
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

3. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
IL 3; supports growth and differentiation of bone marrow stem cells
Anemias (esp due to renal failure)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

4. What does interferon gamma do to be antiviral?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
Increases expression of MHC I and MHC II and also activates NK cells
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

5. What happens in a secondary follicle?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Superficial inguinal
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

6. What are the main symptoms of T cell immunodeficiencies?
Recom IL 11; thrombocytopenia
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Fc
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

7. 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)
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 :(
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

8. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
The patient could become cyanotic in the OR!
A - B - C; all the D's

9. which of the hypersensitivity reactions is not Ab mediated?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Celiac
Type IV

10. when can graft versus host disease? What is the result?
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
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

11. 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
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
isotype
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

12. What is the autoantibody for SLE that is nonspecific? Specific?
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Increases expression of MHC I and MHC II and also activates NK cells
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

13. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Pernicious Anemia and Hashimotos
If there is class switching and plasma cell production (that is when memory cells are produced)

14. What is chronic mucocutaneous candidiasis d/t?
IgE
Liver! (they are proteins circulating in the blood)
T cell dysfunction
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

15. Which disease is associated with B8?
Graves
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
pentamer
The igA found in breast milk

16. are Th cells involved in trapping of antigens of endotoxin/LPS?
CRP - C3b - IgM
Previous transfusion; pregnant woman whose fetus had paternal antigens
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
No because no peptide fragment!

17. What are the autoantibodies for hashimotos?
Anti alpha subunit 3 of collagen on type IV bm
Antimicrosomal and antithyroglobulin
TGF beta and IL 10
Activate macrophages

18. What is the presentation of scid? treatment?
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

19. 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
Activates cytotoxic CD 8 T cells as second signal
type four
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

20. How does complement link innate and adaptive?
Cross link
Hereditary angioedema; PNH
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

21. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Antidote for digoxin intoxication
Alternative splicing of mRNA

22. What is the pathogenesis of a candida skin test?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Delayed type hypersensitivity

23. can igG cross the placenta?
not Ab mediated
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Yes

24. What is the presentation of Brutons agammaglobulinemia?
pale central germinal centers
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Active; passive - fast but short half life (3 weeks!)
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

25. What is filgrastim and sargramostim? and What is it used for?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

26. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
dimer
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

27. Which diseases are associated with DR4?
RNA segment reassortment
Negative nitroblue tetrazolium reduction test
DM type I and RA
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

28. What is the pathogenesis of HyperIgE syndrome? What are the labs?
IL 3; supports growth and differentiation of bone marrow stem cells
Th cells fail to produce interferon gamma; a lot of IgE
MHC I - CD16 - CD56
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

29. What is the clinical use for sirolimus? what should you combine it with?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Anti alpha subunit 3 of collagen on type IV bm
DM type I and RA

30. Name the three opsonins
Stimulate the liver to release acute phase reactants
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
CRP - C3b - IgM

31. What are MHC's necessary for? By themselves?
IgG
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
T cell activation; no with CD 4 or CD 8
Receiving preformed Antibodies

32. 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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
CRP - C3b - IgM

33. Monomer in circulation - ___ when secreted
Popliteal
dimer
Superior mesenteric
IL 4 - 5 - 10 - 6

34. What are the main symptoms of B cell immunodeficiencies?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Negative!
SP infections
IL 3; supports growth and differentiation of bone marrow stem cells

35. What does granulysin do?
Edema and necrosis in that region
Anti alpha subunit 3 of collagen on type IV bm
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

36. What are the mediators that mast cells release?
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
not Ab mediated
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

37. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti mitochondrial
Graves
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a

38. What is the pathogenesis of a hypersensitivity reaction?
Th2; Th1
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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

39. How is i Th1 helper cell inhibited?
Not thymus - BM
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cytokine IL 10 secreted by Th2
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

40. What is the pathology in hyperacute transplant rejection?
Anti Ach receptor
Pernicious Anemia and Hashimotos
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Hereditary angioedema; PNH

41. Which disease is associated with DR7?
Superficial inguinal
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
C5a
Steroid responsive nephrotic syndrome

42. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Paracortex; viral infection
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Antidesmoglein
Influenza; antigenic shift; antigenic drift

43. A lymph node is a ________ lymphoid organ.
secondary
Antihistone
Anemias (esp due to renal failure)
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

44. What are target cells?
heavy chains
T cell precursor
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Cells that stil have weird parts of their membrane that macrophages usually bite off

45. What does interferon gamma do? What two type of cells does it attack mostly?
Remove encapsulated bacateria
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

46. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Activates Th1 helper cells; Macrophages
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Hemochromatosis

47. What can cause a lymph node enlargement?
The patient could become cyanotic in the OR!
IL 5
Local infection/inflammation; infection of the ln itself; metastasis
Daclizumab; prevent ACUTE rejection of renal transplant

48. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
MHC I - CD16 - CD56
By transcytosis
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

49. What is the clinical use of Muromonab?
Humoral
Active; passive - fast but short half life (3 weeks!)
Immunosuppression after kidney transplantation
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. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antidote for digoxin intoxication
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
A chemotactic factor for neutrophils

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