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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.
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. Complements are...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
acute phase reactants
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

2. which antibodies can bind complement?
IL 1 and IL 6
IgM and IgG
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Activates Th1 helper cells; Macrophages

3. The lymphocytes are ________ origin
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Celiac
mesenchymal
NK cells

4. The two heavy chains of an antibody contribute to the...
Fab portion
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
If there is class switching and plasma cell production (that is when memory cells are produced)

5. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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 :(
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Daclizumab; prevent ACUTE rejection of renal transplant
Alternative splicing of mRNA

6. What is the clinical use for azathioprine?
...
opsonizes
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Barrel hoop basement membrane fenestrations

7. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Celiac
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Edema and necrosis in that region

8. T/F B cells do not require a second signal
Anti U1 RNP (ribonucleoprotein)
delayed!
False! B cell class switching requires a second signal
MHC I; from RER with help of the B2 microglobulin

9. What is the toxicity of azathioprine?
A j chain
...
Axillary
Liver! (they are proteins circulating in the blood)

10. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
IgG
All MHC 1/CD8
Its a serine protease that activates apoptosis; NK and CD8
...

11. which B and T cell disorder presents with specifically low IgM?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Wiskott Aldrich syndrome
A - B - C; all the D's

12. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
IL 5
Interferon gamma; Th1
IL 4
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

13. What lymph node drains the breast?
Axillary
Delayed type hypersensitivity
MS - hay fever - SLE - goodpastures
mesenchymal

14. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Hereditary angioedema; PNH
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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

15. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
delayed!
IL 15; IL 12 - interferon Beta and interferon alpha
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

16. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
A - B - C; all the D's

17. What are the PALS?
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 :(
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgE
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

18. How does igA cross the epithelium?
active complement pathway
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgM and IgD
By transcytosis

19. What is oprelevkin? and What is it used for?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Recom IL 11; thrombocytopenia
No because no peptide fragment!

20. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti TSh receptor
The igA found in breast milk

21. ________ regulate the cell mediated response.
Severe pyogenic infections early in life
Anti Jo -1
Anti SS- A (anti RO) and Anti SS- B
Humoral

22. What can cause a lymph node enlargement?
encapsulated
Acts as second signal on B cells to induce class switching to IgE and IgG
Local infection/inflammation; infection of the ln itself; metastasis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

23. What is muromonab - CD3 (OKT3)
Graves
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
RNA segment reassortment
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

24. Type Iv hypersensitivity is...
pentamer
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
delayed!
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

25. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
MHC class molecules bind to KIRS or CD94 to prevent killing
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

26. What are the T cell functions?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Graves
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

27. What is the marginal zone of the spleen? what happens there?
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
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
Antihistone
isotype

28. What type of side chains are found on Fc region of an antibody?
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
Carbohydrate
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

29. What are the autoantibodies for graves?
Acts as second signal on B cells to induce class switching to IgE and IgG
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anti TSh receptor
If there is class switching and plasma cell production (that is when memory cells are produced)

30. What are the autoantibodies for type I diabetes mellitus?
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
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti glutamate carboxylase and anti insulin

31. What is a factor that is a predictor for a bad transplantation?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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!
Rheumatic arthritis

32. What is a type I hypersensitivity reaction? What is atopic?
opsonizes
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
If there is class switching and plasma cell production (that is when memory cells are produced)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

33. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

34. What cytokines to Th2 secrete?
IL 5
Anti smooth muscle
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
IL 4 - 5 - 10 - 6

35. IgE has the ___________ in the serum
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
lowest concentration
The patient could become cyanotic in the OR!
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

36. What is recomb beta interferon used for?
SP infections
Axillary
MS
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

37. What lymph node drains the sigmoid colon?
SP infections
Inferior mesenteric
Influenza; antigenic shift; antigenic drift
Secretory component

38. Describe the Mannose Lectin pathway
CD56
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Yes
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

39. What is the mechanism for sirolimus? what else it known as?
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
IL 4 - 5 - 10 - 6
Superficial inguinal
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

40. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

41. 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?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
neutrophilia!

42. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Internal iliac
Paracortex

43. What are target cells?
cannot cross placenta
Cells that stil have weird parts of their membrane that macrophages usually bite off
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Antibody mediated cytotoxicity; either complement dependent or complement independent

44. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
DM type I

45. What are the autoantibodies for drug induced lupus?
IgG
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Antihistone

46. which cytokine inhibits TH2 cells? secreted by who?
TLR ad nuclear receptors
Activates Th1 helper cells; Macrophages
Interferon gamma; Th1
Severe pyogenic infections early in life

47. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Graves
Not thymus - BM
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

48. How is i Th1 helper cell inhibited?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 5
Cytokine IL 10 secreted by Th2

49. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
Superficial inguinal
CRP - C3b - IgM
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

50. What is the defect in hyper IgM syndrome? What are the lab results?
Daclizumab; prevent ACUTE rejection of renal transplant
Its main effect is a defect in Ab opsonization for killing
SP infections
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E