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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What is the pathogenesis of HyperIgE syndrome? What are the labs?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Pernicious Anemia and Hashimotos
TGF beta and IL 10
Th cells fail to produce interferon gamma; a lot of IgE

2. other than eat and bite RBCs what else do Macrophages of spleen do>
Antibody mediated cytotoxicity; either complement dependent or complement independent
Remove encapsulated bacateria
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
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 :(

3. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Activate macrophages
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

4. What does IL 4 do?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Acts as second signal on B cells to induce class switching to IgE and IgG
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

5. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
A j chain
Antidesmoglein
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

6. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
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
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
Interferon gamma; Th1
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

7. From where do cytokines come from?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Lymphocytes
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

8. What links the adaptive and innate immunity?
Complement activation (active in both)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

9. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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 :(
Delayed type hypersensitivity

10. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Influenza; antigenic shift; antigenic drift
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

11. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Wiskott Aldrich syndrome

12. What do mature naive B lymphocytes express?
acute phase reactants
IgM and IgD
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

13. What is anergy? why does this occur?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Negative!
Sinusitis - otitis media - pneumonia
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

14. can igG cross the placenta?
RNA segment reassortment
Yes
Steroid responsive nephrotic syndrome
IL 15; IL 12 - interferon Beta and interferon alpha

15. What is the main cytokine that activates eosinophils?
IL 5
Rheumatic arthritis
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Inferior mesenteric

16. which B and T cell disorder presents with specifically low IgM?
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
pentamer
Wiskott Aldrich syndrome
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

17. What is the autoantibody for SLE that is nonspecific? Specific?
active complement pathway
Superficial inguinal
CRP - C3b - IgM
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

18. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
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
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

19. What are the two signals required for Th1 cells? what happens after then activated?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cytokine IL 10 secreted by Th2
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti Jo -1

20. The ______ in the BM are DN - the DP are in the cortex of thymus
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
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
Influenza; antigenic shift; antigenic drift
T cell precursor

21. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
TGF beta and IL 10
neutrophilia!

22. which antibodies prevent antigens from binding mucosal surfaces?
IgA
lowest concentration
type four
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

23. What are the main Cell surface proteins on T cells?
Active; passive - fast but short half life (3 weeks!)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Edema and necrosis in that region

24. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Rheumatic arthritis
Glycoproteins; HLA
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

25. What does interferon gamma do to be antiviral?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Bind FcG for antibody dependent cellular cytotoxicity
Barrel hoop basement membrane fenestrations
Increases expression of MHC I and MHC II and also activates NK cells

26. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
isotype
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

27. The two heavy chains of an antibody contribute to the...
Recom IL 11; thrombocytopenia
active complement pathway
Fab portion
Internal iliac

28. What can cause a lymph node enlargement?
Influenza; antigenic shift; antigenic drift
Local infection/inflammation; infection of the ln itself; metastasis
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

29. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
Graves
IgG
MS

30. What is passive immunity?
Receiving preformed Antibodies
Cyclosporine - OKT3
Anti topoisomerase
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

31. What is the clinical use for azathioprine?
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
...
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
acute phase reactants

32. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
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
SP infections
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

33. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Severe pyogenic infections early in life
IgM
Chronic granulomatous disease
Alternative splicing of mRNA

34. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

35. Which is the main antibody that provides passive immunity to infants?
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
S. aureus - E. Coli - aspergillus
IgG
heavy chains

36. What are the autoantibodies for Celiac disease?
Anti TSh receptor
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
TLR ad nuclear receptors

37. where are complements produced?
Liver! (they are proteins circulating in the blood)
Paracortex; viral infection
TNF alpha and IL1
Barrel hoop basement membrane fenestrations

38. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
dimer
Delayed type hypersensitivity
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

39. How is the thymus organized? what happens in each section?
Antidote for digoxin intoxication
C5a
IgM and IgA
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

40. What does granulysin do?
Receiving preformed Antibodies
Hereditary angioedema; PNH
False! B cell class switching requires a second signal
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

41. What lymph node drains the lateral side of the dorsum of the foot?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Popliteal
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
Anti smooth muscle

42. What is the pathogenesis of acute transplant rejection? When does it occur?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
...

43. where do NK cells develop?
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
2 heavy chains and two light chains
Not thymus - BM
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

44. What is chronic mucocutaneous candidiasis d/t?
By transcytosis
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
Pernicious Anemia and Hashimotos
T cell dysfunction

45. what characterizes an arthus reaction?
No because no peptide fragment!
Edema and necrosis in that region
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)
Fc

46. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Anti SS- A (anti RO) and Anti SS- B
Immunosuppression after kidney transplantation
MHC I; from RER with help of the B2 microglobulin
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t

47. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IL 3; supports growth and differentiation of bone marrow stem cells
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

48. What happens in a secondary follicle?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Glycoproteins; HLA
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

49. What is the pathology of acute transplant rejection? is it reversible?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Interferon gamma and IL 2
Anti TSh receptor
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

50. Which type of selection of thymic development provides central tolerance?
Negative selection
Pernicious Anemia and Hashimotos
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
IgE

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USMLE Step 1 Immunology

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