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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. what ensure that a memory response is generated?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IL 3; supports growth and differentiation of bone marrow stem cells
Immunoflourescent staining of tissue biopsies
If there is class switching and plasma cell production (that is when memory cells are produced)

2. which cells have more complete tolerance - B or T cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
T
MHC I - CD16 - CD56
Anti glutamate carboxylase and anti insulin

3. are Th cells involved in trapping of antigens of endotoxin/LPS?
secondary
No because no peptide fragment!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antihistone

4. What is the toxicity of muromonab?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Superior mesenteric
Activates cytotoxic CD 8 T cells as second signal

5. What is epo used for?
Anemias (esp due to renal failure)
CRP - C3b - IgM
MHC class molecules bind to KIRS or CD94 to prevent killing
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs

6. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
IL 5
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Axillary
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

7. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti smooth muscle
Activates Th1 helper cells; Macrophages
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

8. Which MHC presents intracellular peptides? how so?
cannot cross placenta
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)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC I; from RER with help of the B2 microglobulin

9. What are the function of B cells?
Recom IL 11; thrombocytopenia
Fc
Delayed type hypersensitivity
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

10. Which diseases are associated with DR5?
Th cells fail to produce interferon gamma; a lot of IgE
Pernicious Anemia and Hashimotos
IgE
Anti topoisomerase

11. IgM can fix complement but...
mesenchymal
A recomb cytokine of IL 2; RCC and metastatic melanoma
cannot cross placenta
By transcytosis

12. From where do cytokines come from?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Delayed type hypersensitivity
Lymphocytes
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

13. What is the main cytokine that activates eosinophils?
Liver! (they are proteins circulating in the blood)
Antihistone
IL 5
Superficial inguinal

14. What are the autoantibodies for goodpastures syndrome?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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 alpha subunit 3 of collagen on type IV bm
IL 15; IL 12 - interferon Beta and interferon alpha

15. What is the main function of IL 12? other than macrophages who else can release IL 12?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

16. What lymph node drains the scrotum?
CD56
Superficial inguinal
The patient could become cyanotic in the OR!
Inferior mesenteric

17. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Alternative splicing of mRNA
Rheumatic arthritis
...
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

18. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
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

19. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Cross link
Active; passive - fast but short half life (3 weeks!)
Not thymus - BM

20. What is the defect in hyper IgM syndrome? What are the lab results?
Acts as second signal on B cells to induce class switching to IgE and IgG
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

21. How does complement link innate and adaptive?
The patient could become cyanotic in the OR!
Antibody mediated cytotoxicity; either complement dependent or complement independent
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Antidote for digoxin intoxication

22. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Para aortic
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
If there is class switching and plasma cell production (that is when memory cells are produced)

23. What is the general structure of an Ab?
Its main effect is a defect in Ab opsonization for killing
2 heavy chains and two light chains
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
RNA segment reassortment

24. 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).
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Acts as second signal on B cells to induce class switching to IgE and IgG
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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!

25. What does interferon gamma do? What two type of cells does it attack mostly?
Anti Jo -1
MHC class molecules bind to KIRS or CD94 to prevent killing
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

26. 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?
Edema and necrosis in that region
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

27. Describe the complement independent Type II hypersenstivity reaction. Give an example.
secondary
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Antidote for digoxin intoxication
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

28. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Humoral
Anti TSh receptor
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

29. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Hemochromatosis
Liver! (they are proteins circulating in the blood)

30. What is the receptor for EBV? On what cells is that located?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
CD21 on B cells (although there is T cell lymphocytosis in EBV)

31. What is recomb gamma interferon used for?
A chemotactic factor for neutrophils
Chronic granulomatous disease
Anti IF
pale central germinal centers

32. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
A - B - C; all the D's
The igA found in breast milk
Humoral

33. What is the main function of TNF alpha? How does it do this?
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
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
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

34. IgM can exist as a _______ also
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
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

35. What is the presentation of common variable immunodef? and What are the labs?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
MS
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

36. What is three common causes of severe combined immunodef? What is the result of all three?
except hyperacute
Delayed type hypersensitivity
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Antimicrosomal and antithyroglobulin

37. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
dimer
Liver! (they are proteins circulating in the blood)
Anti IF

38. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
IL 5
type four
Influenza; antigenic shift; antigenic drift
Severe pyogenic infections early in life

39. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti glutamate carboxylase and anti insulin
active complement pathway

40. To what portion of the Antibody do the complements bind?
Fc
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

41. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Its main effect is a defect in Ab opsonization for killing
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Paracortex
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

42. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

43. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Not thymus - BM
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Viral neutralization of igM and IgG!

44. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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 :(
Influenza; antigenic shift; antigenic drift
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

45. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
acute phase reactants
Influenza; antigenic shift; antigenic drift
CD21 on B cells (although there is T cell lymphocytosis in EBV)

46. is IgM an opsonizer?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Negative!
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
pentamer

47. What is the most common selective Ig deficiency? What is the presentation?
except hyperacute
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

48. where do somatic hypermutation and class switching occur?
Anti Ach receptor
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
In the germinal center of secondary follicles (In the paler center)
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

49. What are the autoantibodies for graves?
Immunoflourescent staining of tissue biopsies
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Anti TSh receptor
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

50. What is the pathogenesis of a candida skin test?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Increases expression of MHC I and MHC II and also activates NK cells
Delayed type hypersensitivity
Tetanus - Botulinum - HBV - Rabies

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USMLE Step 1 Immunology

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