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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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1. What lymph node drains the rectum (above the pectinate line)?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Internal iliac
IgM and IgD
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

2. What is the pathology of acute transplant rejection? is it reversible?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
IgM
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
not Ab mediated

3. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
T cell activation; no with CD 4 or CD 8
Glycoproteins; HLA
Wiskott Aldrich syndrome
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

4. What are the main Cell surface proteins on T cells?
Hemochromatosis
Lymphocytes
A - B - C; all the D's
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

5. A lymph node is a ________ lymphoid organ.
Rheumatic arthritis
secondary
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Anti glutamate carboxylase and anti insulin

6. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgE
Antihistone

7. How is sirolimus different from tacrolimus?
No because no peptide fragment!
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Paracortex
Anti Ach receptor

8. How fast does it occur?
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
Lymphocytes
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
The patient could become cyanotic in the OR!

9. Which diseases are associated with DR2?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
NK cells
MS - hay fever - SLE - goodpastures

10. What is a type I hypersensitivity reaction? What is atopic?
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
Its main effect is a defect in Ab opsonization for killing
DM type I
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

11. Name two endogenous pyrogens
IgM and IgG
opsonizes
Not thymus - BM
IL 1 and IL 6

12. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Wiskott Aldrich syndrome
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h

13. What does interferon gamma do to be antiviral?
Cross link
Increases expression of MHC I and MHC II and also activates NK cells
Secretory component
pathogenesis

14. What are the autoantibodies for Celiac disease?
active complement pathway
IL 1 and IL 6
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

15. What bugs can actually infect the lymph node itself?
...
opsonizes
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

16. What are the main symptoms of T cell immunodeficiencies?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Barrel hoop basement membrane fenestrations

17. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Negative selection
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

18. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
The patient could become cyanotic in the OR!
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Its main effect is a defect in Ab opsonization for killing
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

19. What are the autoantibodies for graves?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti TSh receptor
Paracortex
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

20. What lymph node drains the stomach?
...
Celiac
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
secondary

21. IgE has the ___________ in the serum
Cytokine IL 10 secreted by Th2
lowest concentration
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
MHC class molecules bind to KIRS or CD94 to prevent killing

22. Which is the most abundant antibody in blood?
IgG
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
B - T - and NK cells
Celiac

23. what bacteria are a splenectomy patient most susceptible to? why?
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
Remove encapsulated bacateria
dimer
False! B cell class switching requires a second signal

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

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25. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
type four
IgA
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

26. What are the mediators that mast cells release?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
The patient could become cyanotic in the OR!
Anti glutamate carboxylase and anti insulin
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

27. What does CD16 on NK cells do?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Basophils! THey want IG E class switch!
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
Bind FcG for antibody dependent cellular cytotoxicity

28. What is colostrum?
Th2; Th1
The igA found in breast milk
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
...

29. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

30. What does granzyme do? who secretes it?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
A chemotactic factor for neutrophils
pathogenesis
Its a serine protease that activates apoptosis; NK and CD8

31. What does IL 2 do?
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
Activates cytotoxic CD 8 T cells as second signal
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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

32. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
A recomb cytokine of IL 2; RCC and metastatic melanoma
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

33. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Antimicrosomal and antithyroglobulin
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
CD56

34. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Wiskott Aldrich syndrome
neutrophilia!
Superior mesenteric
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

35. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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!
IL 15; IL 12 - interferon Beta and interferon alpha

36. How does igA cross the epithelium?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
By transcytosis
IgA
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

37. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Its a serine protease that activates apoptosis; NK and CD8
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Hereditary angioedema; PNH
pentamer

38. What is the pathogenesis of a hypersensitivity reaction?
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
Th cells fail to produce interferon gamma; a lot of IgE
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

39. What are the major functions of Antibodies?
All MHC 1/CD8
IgM
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
No because no peptide fragment!

40. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
...
Barrel hoop basement membrane fenestrations
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
TNF alpha and IL1

41. What lymph node drains the sigmoid colon?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
T
IgM and IgG
Inferior mesenteric

42. What is the general structure of an Ab?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Axillary
2 heavy chains and two light chains
Not thymus - BM

43. What does IgA pick up from epithelial cells before being secreted?
IgAs in mothers breast milk!
Secretory component
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 antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

44. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Stimulate the liver to release acute phase reactants
acute phase reactants
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

45. Describe the Mannose Lectin pathway
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Steroid responsive nephrotic syndrome

46. What is the treatment of acute transplant rejection?
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
Cyclosporine - OKT3
A recomb cytokine of IL 2; RCC and metastatic melanoma
NK cells

47. What are superantigens? give two examples.
RNA segment reassortment
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
Yes
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

48. can igG cross the placenta?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Yes

49. which of the hypersensitivity reactions is not Ab mediated?
Type IV
Remove encapsulated bacateria
...
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

50. What does IL 5 do?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

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USMLE Step 1 Immunology

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