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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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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 mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
IgM and IgD
Histamine; post capillary venules - vasodilation
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

2. which of the transplant rejections is antibody mediated? why does it occur?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Rheumatic arthritis
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Secretory component

3. hat is the presentation of Jobs syndrome or Hyper IgE?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
When you select for which MHC it will have; take out the lymphs that self react
Chronic granulomatous disease

4. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Anemias (esp due to renal failure)
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
MHC class molecules bind to KIRS or CD94 to prevent killing
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

5. Other than stimulating fever - what else does IL 6 do?
Axillary
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Stimulate the liver to release acute phase reactants
Basophils! THey want IG E class switch!

6. Which disease is associated with HLA A3?
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)
IgM and IgG
Hemochromatosis

7. What is the main function of interferons?
Anti Jo -1
Recom IL 11; thrombocytopenia
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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

8. What is hereditary angioedema? What are the C3 levels?
S. aureus - E. Coli - aspergillus
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
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
Delayed type hypersensitivity

9. What are the autoantibodies for type I diabetes mellitus?
mesenchymal
Anti glutamate carboxylase and anti insulin
Antidesmoglein
Its main effect is a defect in Ab opsonization for killing

10. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
S. aureus - E. Coli - aspergillus
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

11. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
IgG
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

12. What is filgrastim and sargramostim? and What is it used for?
Its a serine protease that activates apoptosis; NK and CD8
NK cells
Delayed type hypersensitivity
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

13. The idiotype; the Fc portion determines the...
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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)
isotype
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

14. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
heavy chains
Anti alpha subunit 3 of collagen on type IV bm
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

15. What are the three types of lymphocytes?
B - T - and NK cells
Superficial inguinal
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
...

16. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
type four
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
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

17. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
MS - hay fever - SLE - goodpastures
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)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

18. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
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
dimer
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

19. Name the three opsonins
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Macrophages - Dendritic cells - B cells
CRP - C3b - IgM
heavy chains

20. what cytokine does basophils secrete?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 4

21. What type of side chains are found on Fc region of an antibody?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Carbohydrate
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Cells that stil have weird parts of their membrane that macrophages usually bite off

22. What happens in a deficiency of C3?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
Anemias (esp due to renal failure)

23. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgM and IgD
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

24. What is the white pulp of the spleen?
Sinusitis - otitis media - pneumonia
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
pentamer

25. What does granzyme do? who secretes it?
Superficial inguinal
Its a serine protease that activates apoptosis; NK and CD8
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Axillary

26. what cell surface marker is used for NK cells as it is unique to them?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
heavy chains
CD56
Humoral

27. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Antibody mediated cytotoxicity; either complement dependent or complement independent
IL 4
Previous transfusion; pregnant woman whose fetus had paternal antigens

28. What is a type I hypersensitivity reaction? What is atopic?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Antihistone
Negative nitroblue tetrazolium reduction test

29. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Cross link
IgA
Superior mesenteric
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

30. what will NK cells do to cells covered in IgG Ab? why?
Edema and necrosis in that region
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Kill them because they have CD16 on them that recognize the FcG portion

31. what cell surface proteins are on all APCs?
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
pentamer
delayed!
MHC II - B7

32. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
...

33. What is the main cytokine that activates eosinophils?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
lowest concentration
IL 5

34. What is the most common selective Ig deficiency? What is the presentation?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Paracortex; viral infection

35. What is digoxin immune Fab used for?
IgG
Antidote for digoxin intoxication
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IL 4 - 5 - 10 - 6

36. What is the cause of thymic aplasia? What is its presentation? What are the labs?
MS - hay fever - SLE - goodpastures
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
TGF beta and IL 10
Previous transfusion; pregnant woman whose fetus had paternal antigens

37. Describe complement dependent Type II hypersensitivity. Give an example.
Carbohydrate
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
Barrel hoop basement membrane fenestrations
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

38. What are MHC's necessary for? By themselves?
Internal iliac
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
T cell activation; no with CD 4 or CD 8
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

39. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Interferon gamma; Th1
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant

40. What are the PALS?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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!

41. What are the main cell surface proteins on B cells?
Influenza; antigenic shift; antigenic drift
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
acute phase reactants
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

42. What are the autoantibodies for drug induced lupus?
A - B - C; all the D's
Anti mitochondrial
Antihistone
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

43. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
carboxy terminal
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

44. What is the presentation of scid? treatment?
Tetanus - Botulinum - HBV - Rabies
pale central germinal centers
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

45. The alternative pathway is the only constutively...
Cells that stil have weird parts of their membrane that macrophages usually bite off
active complement pathway
Antidesmoglein
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

46. where are complements produced?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Liver! (they are proteins circulating in the blood)
The igA found in breast milk
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

47. What is recomb beta interferon used for?
MS
IL 1 and IL 6
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

48. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
RNA segment reassortment
Anti glutamate carboxylase and anti insulin
Immunoflourescent staining of tissue biopsies
TNF alpha and IL1

49. which antibodies can bind complement?
Its main effect is a defect in Ab opsonization for killing
IgM and IgG
Acts as second signal on B cells to induce class switching to IgE and IgG
lowest concentration

50. What does IL 5 do?
TGF beta and IL 10
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Stimulate the liver to release acute phase reactants
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

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