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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
Alternative splicing of mRNA
IL 4 - 5 - 10 - 6
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

2. So antibodies are the effectors for the humoral response. List some of their functions.
Macrophages - Dendritic cells - B cells
Humoral
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

3. Only the _______ contribute to the Fc region
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!
heavy chains
not Ab mediated
Activate macrophages

4. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
acute phase reactants
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

5. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Humoral
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Cross link
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)

6. which type of immunity is slow but long lasting? as opposed to...
Immunosuppression after kidney transplantation
Rheumatic arthritis
Active; passive - fast but short half life (3 weeks!)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

7. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
C5a
MS
A recomb cytokine of IL 2; RCC and metastatic melanoma
Its main effect is a defect in Ab opsonization for killing

8. What is the autoantibody for SLE that is nonspecific? Specific?
Axillary
T cell activation; no with CD 4 or CD 8
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

9. What is the main function of IL 12? other than macrophages who else can release IL 12?
Anti U1 RNP (ribonucleoprotein)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Active; passive - fast but short half life (3 weeks!)

10. What is serum sickness? give an example.
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
Carbohydrate
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Superior mesenteric

11. What are the three types of lymphocytes?
Barrel hoop basement membrane fenestrations
Cells that stil have weird parts of their membrane that macrophages usually bite off
SP infections
B - T - and NK cells

12. How fast does it occur?
Antidote for digoxin intoxication
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
The patient could become cyanotic in the OR!

13. what characterizes an arthus reaction?
T
Fab portion
not Ab mediated
Edema and necrosis in that region

14. Describe the complement independent Type II hypersenstivity reaction. Give an example.
dimer
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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

15. Which disease is associated with B8?
Graves
heavy chains
Anti smooth muscle
Wiskott Aldrich syndrome

16. What is the main cytokine released by T cells? What does it do
IL 15; IL 12 - interferon Beta and interferon alpha
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IL 3; supports growth and differentiation of bone marrow stem cells
Anti U1 RNP (ribonucleoprotein)

17. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Celiac
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
All MHC 1/CD8
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

18. From where do cytokines come from?
MHC class molecules bind to KIRS or CD94 to prevent killing
Lymphocytes
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
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

19. are Th cells involved in trapping of antigens of endotoxin/LPS?
secondary
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
No because no peptide fragment!

20. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Its main effect is a defect in Ab opsonization for killing
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

21. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Chronic granulomatous disease
NK cells
DM type I and RA

22. What is the presentation of hyperIgM syndrome?
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Severe pyogenic infections early in life

23. What is the pathology seen in chronic transplant rejection?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
T cell dysfunction
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
T cell precursor

24. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Interferon gamma and IL 2
delayed!
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

25. How is sirolimus different from tacrolimus?
Antidote for digoxin intoxication
...
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

26. IgM can exist as a _______ also
IL 15; IL 12 - interferon Beta and interferon alpha
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
pentamer
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

27. What is Aldesleukin? What is it used for
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Yes

28. where do NK cells develop?
Yes
Not thymus - BM
Fab portion
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

29. What does IL 2 do?
IgG
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Activates cytotoxic CD 8 T cells as second signal
RNA segment reassortment

30. For which toxins are preformed antibodies (passive) given?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgM and IgG
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
Tetanus - Botulinum - HBV - Rabies

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

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32. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Anti topoisomerase
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Edema and necrosis in that region

33. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Paracortex; viral infection
Macrophages - Dendritic cells - B cells

34. 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
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!
Graves
T cell dysfunction

35. 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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
pale central germinal centers
Active; passive - fast but short half life (3 weeks!)

36. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti viral and anti tumor
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

37. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Cytokine IL 10 secreted by Th2
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Not thymus - BM

38. How is i Th1 helper cell inhibited?
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
Anti Jo -1
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Cytokine IL 10 secreted by Th2

39. What is recomb gamma interferon used for?
Chronic granulomatous disease
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
False! B cell class switching requires a second signal
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

40. Name 5 ways Antibody diversity is generated?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Popliteal
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
pale central germinal centers

41. What is an example of a parasite showing antigenic variation?
Stimulate the liver to release acute phase reactants
except hyperacute
Lymphocytes
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

42. What can cause a lymph node enlargement?
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
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
Local infection/inflammation; infection of the ln itself; metastasis
Paracortex

43. What kinds of receptors activate innate immunity?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
IgM and IgG
TLR ad nuclear receptors

44. What lymph node drains the lateral side of the dorsum of the foot?
Chronic granulomatous disease
Hereditary angioedema; PNH
Popliteal
IgG

45. describe the classic complement pathway.
IgM and IgA
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
In the germinal center of secondary follicles (In the paler center)

46. what prevents NK cells from killing normal cells if their default is to kill?
Paracortex
MHC class molecules bind to KIRS or CD94 to prevent killing
Liver! (they are proteins circulating in the blood)
C5a

47. How is the thymus organized? what happens in each section?
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
IL 15; IL 12 - interferon Beta and interferon alpha

48. What lymph node drains the testes?
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
Para aortic
Graves
Negative!

49. 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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Popliteal
MHC I - CD16 - CD56

50. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Severe pyogenic infections early in life
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
Activate macrophages
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens