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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 are the main Cell surface proteins on T cells?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Tetanus - Botulinum - HBV - Rabies
Inferior mesenteric
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

2. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Rheumatic arthritis
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Lymphocytes

3. what ensure that a memory response is generated?
Th cells fail to produce interferon gamma; a lot of IgE
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
If there is class switching and plasma cell production (that is when memory cells are produced)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

4. Which disease is associated with HLA A3?
Antihistone
The patient could become cyanotic in the OR!
Hemochromatosis
A recomb cytokine of IL 2; RCC and metastatic melanoma

5. A lymph node is a ________ lymphoid organ.
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IL 4 - 5 - 10 - 6
secondary
delayed!

6. What is the main function of IL 8?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
A chemotactic factor for neutrophils
Severe pyogenic infections early in life

7. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
...
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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

8. Only the _______ contribute to the Fc region
heavy chains
Anti SS- A (anti RO) and Anti SS- B
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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

9. which cytokine inhibits TH2 cells? secreted by who?
Paracortex
Secretory component
Interferon gamma; Th1
carboxy terminal

10. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
In the germinal center of secondary follicles (In the paler center)
Severe pyogenic infections early in life
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

11. What are the autoantibodies for wegeners granulomatosis?
dimer
...
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

12. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgM and IgG

13. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Antihistone
Acts as second signal on B cells to induce class switching to IgE and IgG

14. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
encapsulated
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

15. What are the autoantibodies for autoimmune hepatitis?
Th2; Th1
Anti smooth muscle
Anti SS- A (anti RO) and Anti SS- B
Anti IF

16. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Wiskott Aldrich syndrome
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
IgE

17. 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?
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
Superficial inguinal
IL 5
Immunoflourescent staining of tissue biopsies

18. What are the main symptoms of B cell immunodeficiencies?
secondary
Histamine; post capillary venules - vasodilation
SP infections
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

19. What are howell jolly bodies?
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IgG

20. The pathogenesis of contact dermatitis is ________ hypersensitivity
T cell dysfunction
type four
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
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

21. What is the marginal zone of the spleen? what happens there?
Superficial inguinal
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
Kill them because they have CD16 on them that recognize the FcG portion

22. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
acute phase reactants
Anti Ach receptor
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

23. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Th2; Th1
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

24. What does granulysin do?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
lowest concentration

25. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Fc

26. What is thrombopoietin used for?
A chemotactic factor for neutrophils
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Thrombocytopenia
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

27. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cyclosporine - OKT3
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 :(
Edema and necrosis in that region

28. What is colostrum?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
The igA found in breast milk

29. What is the receptor for EBV? On what cells is that located?
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!
B - T - and NK cells
CD21 on B cells (although there is T cell lymphocytosis in EBV)
pale central germinal centers

30. What is the pathogenesis of a candida skin test?
Edema and necrosis in that region
Delayed type hypersensitivity
T cell dysfunction
CD56

31. what secretes IL 4?
except hyperacute
Basophils! THey want IG E class switch!
encapsulated
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

32. What is immune complex disease? give an example.
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
secondary
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Barrel hoop basement membrane fenestrations

33. What is the presentation of common variable immunodef? and What are the labs?
Edema and necrosis in that region
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Interferon gamma and IL 2

34. In general What are T cells good for?
Anti viral and anti tumor
Pernicious Anemia and Hashimotos
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
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

35. What is filgrastim and sargramostim? and What is it used for?
Rheumatic arthritis
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

36. What is the pathology of acute transplant rejection? is it reversible?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Th2; Th1
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Its a serine protease that activates apoptosis; NK and CD8

37. Describe the Mannose Lectin pathway
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
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
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
CRP - C3b - IgM

38. What is the pathogenesis of HyperIgE syndrome? What are the labs?
neutrophilia!
Humoral
Th cells fail to produce interferon gamma; a lot of IgE
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

39. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antidesmoglein
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

40. What is the toxicity of azathioprine?
...
IL 4 - 5 - 10 - 6
Anti Ach receptor
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

41. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Cross link

42. What are some sinopulmonary infections?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Sinusitis - otitis media - pneumonia
Recom IL 11; thrombocytopenia
C5a

43. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Activates Th1 helper cells; Macrophages
IgE; by activating eosinophils
Basophils! THey want IG E class switch!
Alternative splicing of mRNA

44. Type IV hypersensitivity is i...
not Ab mediated
S. aureus - E. Coli - aspergillus
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Negative selection

45. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Anti Jo -1
IL 4 - 5 - 10 - 6
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
secondary

46. IgG...
Popliteal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
opsonizes

47. What does IgA pick up from epithelial cells before being secreted?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IL 1 and IL 6
Yes
Secretory component

48. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
If there is class switching and plasma cell production (that is when memory cells are produced)
T cell activation; no with CD 4 or CD 8
carboxy terminal
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

49. Which diseases are associated with DR2?
Interferon gamma and IL 2
RNA segment reassortment
Anti topoisomerase
MS - hay fever - SLE - goodpastures

50. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
MS - hay fever - SLE - goodpastures
Antimicrosomal and antithyroglobulin
By transcytosis

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USMLE Step 1 Immunology

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