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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. what results in symptoms of shock in an acute hemolytic transfusion reaction?
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antibody mediated cytotoxicity; either complement dependent or complement independent

2. which antibody activate mast cells - basophils - and eosinophils?
dimer
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IgE
When you select for which MHC it will have; take out the lymphs that self react

3. What is immune complex disease? give an example.
Anti mitochondrial
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Negative!
Tetanus - Botulinum - HBV - Rabies

4. Leukocyte adhesion defect presents with...
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Kill them because they have CD16 on them that recognize the FcG portion
neutrophilia!

5. Describe the complement independent Type II hypersenstivity reaction. Give an example.
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Histamine; post capillary venules - vasodilation
Cells that stil have weird parts of their membrane that macrophages usually bite off

6. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Cross link
Previous transfusion; pregnant woman whose fetus had paternal antigens
T

7. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
RNA segment reassortment
Popliteal
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

8. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Graves
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
pentamer

9. What does IL 5 do?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IL 5
type four
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

10. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
secondary
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
not Ab mediated
All MHC 1/CD8

11. What is the general structure of an Ab?
CRP - C3b - IgM
Paracortex
2 heavy chains and two light chains
Popliteal

12. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
opsonizes
IgM

13. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
A chemotactic factor for neutrophils
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

14. The Fc region is found on the...
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
carboxy terminal

15. which antibody is involved in the primary response or immediate response to an antigen?
IL 4 - 5 - 10 - 6
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgM
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

16. Which antibody mediates immunity to worms? how?
Anti Ach receptor
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
IgE; by activating eosinophils

17. How do you test for type III hypersensitivity?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Immunoflourescent staining of tissue biopsies
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

18. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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 :(
CRP - C3b - IgM
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
A j chain

19. What happens in a deficiency of C3?
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
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

20. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
The igA found in breast milk
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

21. What are superantigens? give two examples.
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
Anti TSh receptor

22. give an example of how influenza does a major antigenic shift.
IL 3; supports growth and differentiation of bone marrow stem cells
A chemotactic factor for neutrophils
RNA segment reassortment
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

23. How does complement link innate and adaptive?
mesenchymal
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
The patient could become cyanotic in the OR!

24. From where do cytokines come from?
type four
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
Lymphocytes
Receiving preformed Antibodies

25. what prevents NK cells from killing normal cells if their default is to kill?
S. aureus - E. Coli - aspergillus
MHC class molecules bind to KIRS or CD94 to prevent killing
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

26. What are target cells?
False! B cell class switching requires a second signal
Anti U1 RNP (ribonucleoprotein)
Cells that stil have weird parts of their membrane that macrophages usually bite off
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

27. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
IgM and IgA
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
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

28. What are the symptoms of serum sickness?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgE
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti TSh receptor

29. What is recomb gamma interferon used for?
C5a
Hereditary angioedema; PNH
Chronic granulomatous disease
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

30. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lymphocytes
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IgM

31. Describe complement dependent Type II hypersensitivity. Give an example.
Carbohydrate
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

32. What is a type I hypersensitivity reaction? What is atopic?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Kill them because they have CD16 on them that recognize the FcG portion
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
T

33. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
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 :(
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
Paracortex; viral infection

34. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 15; IL 12 - interferon Beta and interferon alpha
Cross link

35. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Not thymus - BM
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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!
By transcytosis

36. Which disease is associated with DR7?
Interferon gamma and IL 2
Steroid responsive nephrotic syndrome
Rheumatic arthritis
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

37. What type of fenestrations are found in the red pulp of the spleen?
IgA
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Barrel hoop basement membrane fenestrations
Hemochromatosis

38. What does IL 4 do?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Not thymus - BM
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Acts as second signal on B cells to induce class switching to IgE and IgG

39. What does IL 10 do? who is secreted by?
Anti viral and anti tumor
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T 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
Remove encapsulated bacateria

40. What are the two signals to kill for NK cells?
Receiving preformed Antibodies
Activates cytotoxic CD 8 T cells as second signal
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Interferon gamma; Th1

41. What are the autoantibodies for graves?
Fc
MHC I; from RER with help of the B2 microglobulin
Anti TSh receptor
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

42. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti mitochondrial
Chronic granulomatous disease
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

43. What are the two signals required for T cells? what happens after?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Kill them because they have CD16 on them that recognize the FcG portion
Popliteal

44. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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 :(
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
Not thymus - BM

45. What is hereditary angioedema? What are the C3 levels?
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

46. Type IV hypersensitivity is i...
A - B - C; all the D's
not Ab mediated
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

47. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
...
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

48. __________ are a part of the innate system.
Negative nitroblue tetrazolium reduction test
Axillary
NK cells
TGF beta and IL 10

49. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
MS
IL 4
Celiac
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

50. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
Yes
pentamer