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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.
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1. What lymph node drains the duodenum - jejunum?
Steroid responsive nephrotic syndrome
Superior mesenteric
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

2. How does the alternative pathway lead to MAC activation?
Anti glutamate carboxylase and anti insulin
delayed!
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

3. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
TLR ad nuclear receptors
Its a serine protease that activates apoptosis; NK and CD8

4. IgM can exist as a _______ also
pentamer
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
TLR ad nuclear receptors
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

5. What is the presentation of common variable immunodef? and What are the labs?
active complement pathway
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
IgM and IgA
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

6. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
MS - hay fever - SLE - goodpastures
B - T - and NK cells

7. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Negative nitroblue tetrazolium reduction test
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
Anemias (esp due to renal failure)

8. What are the autoantibodies for drug induced lupus?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antihistone
Para aortic
The igA found in breast milk

9. 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?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MS
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

10. Name the three opsonins
neutrophilia!
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
CRP - C3b - IgM
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

11. Which HLA's are included in MHC I? MHC II?

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12. What happens in a secondary follicle?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

13. What are the autoantibodies for type I diabetes mellitus?
Hemochromatosis
A chemotactic factor for neutrophils
Anti glutamate carboxylase and anti insulin
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

14. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
CRP - C3b - IgM
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Pernicious Anemia and Hashimotos

15. 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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti viral and anti tumor
Kill them because they have CD16 on them that recognize the FcG portion

16. What are the cell surface proteins for Macrophages? which two are for opsonins?
TLR ad nuclear receptors
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

17. Describe complement dependent Type II hypersensitivity. Give an example.
IgE
Popliteal
Fc
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

18. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
type four
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
T
Histamine; post capillary venules - vasodilation

19. What links the adaptive and innate immunity?
Yes
Complement activation (active in both)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
TLR ad nuclear receptors

20. What are the two signals to kill for NK cells?
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti viral and anti tumor
T cell dysfunction

21. What type of fenestrations are found in the red pulp of the spleen?
Acts as second signal on B cells to induce class switching to IgE and IgG
Barrel hoop basement membrane fenestrations
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
mesenchymal

22. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Remove encapsulated bacateria
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
isotype

23. What is the marginal zone of the spleen? what happens there?
IL 4 - 5 - 10 - 6
RNA segment reassortment
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

24. How does complement link innate and adaptive?
Activate macrophages
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
A chemotactic factor for neutrophils
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

25. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Paracortex
Lymphocytes
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
DM type I and RA

26. What is the defect in hyper IgM syndrome? What are the lab results?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
pentamer
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

27. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Interferon gamma; Th1
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Cross link
TNF alpha and IL1

28. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MHC I; from RER with help of the B2 microglobulin
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
Cross link

29. What is Aldesleukin? What is it used for
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
pale central germinal centers
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
A recomb cytokine of IL 2; RCC and metastatic melanoma

30. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Anti TSh receptor
Wiskott Aldrich syndrome
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

31. what mediates the type II hypersensitivity? What are the two different methods?
MHC I; from RER with help of the B2 microglobulin
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

32. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Delayed type hypersensitivity
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

33. What is three common causes of severe combined immunodef? What is the result of all three?
pale central germinal centers
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
IgA
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

34. To what portion of the Antibody do the complements bind?
Anti glutamate carboxylase and anti insulin
Fc
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

35. Other than stimulating fever - what else does IL 6 do?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
type four
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Stimulate the liver to release acute phase reactants

36. What does it mean if there are igM in the serum at birth?
T cell precursor
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Hereditary angioedema; PNH

37. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
SP infections

38. what prevents NK cells from killing normal cells if their default is to kill?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
MHC class molecules bind to KIRS or CD94 to prevent killing
except hyperacute
DM type I and RA

39. Which diseases are associated with DR4?
IgE
RNA segment reassortment
Axillary
DM type I and RA

40. How is i Th1 helper cell inhibited?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
MHC class molecules bind to KIRS or CD94 to prevent killing
Cytokine IL 10 secreted by Th2
Immunosuppression after kidney transplantation

41. Which disease is associated withB B27?
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
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Interferon gamma; Th1

42. What are the autoantibodies for primary biliary cirrhosis?
2 heavy chains and two light chains
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti mitochondrial
Its main effect is a defect in Ab opsonization for killing

43. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
Kill them because they have CD16 on them that recognize the FcG portion
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
A - B - C; all the D's

44. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Active; passive - fast but short half life (3 weeks!)

45. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
By transcytosis

46. From where do cytokines come from?
Lymphocytes
IL 4 - 5 - 10 - 6
T cell precursor
Negative!

47. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Severe pyogenic infections early in life

48. What are four results of a splenectomy?
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
Local infection/inflammation; infection of the ln itself; metastasis
Anemias (esp due to renal failure)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

49. Which diseases are associated with DR2?
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MS - hay fever - SLE - goodpastures
IL 1 and IL 6

50. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Fc
DM type I and RA
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

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USMLE Step 1 Immunology

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