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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
Subjects
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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. What does it mean if there are igM in the serum at birth?
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
MHC class molecules bind to KIRS or CD94 to prevent killing
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
2. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Yes
Antimicrosomal and antithyroglobulin
In the germinal center of secondary follicles (In the paler center)
3. where do NK cells develop?
Axillary
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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)
Not thymus - BM
4. can igG cross the placenta?
Yes
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
5. What are the autoantibodies for type I diabetes mellitus?
Basophils! THey want IG E class switch!
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
Anti glutamate carboxylase and anti insulin
Bind FcG for antibody dependent cellular cytotoxicity
6. Name the three opsonins
opsonizes
CRP - C3b - IgM
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
7. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
IgE; by activating eosinophils
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Influenza; antigenic shift; antigenic drift
Alternative splicing of mRNA
8. What is the clinical use for azathioprine?
RNA segment reassortment
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
...
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
9. What are some catalase positive organisms?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
opsonizes
S. aureus - E. Coli - aspergillus
Hemochromatosis
10. in which immunodef order do you see a lot of pus? no pus?
IgG
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Complement activation (active in both)
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
11. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Superficial inguinal
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
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
12. what mediates the type II hypersensitivity? What are the two different methods?
T cell activation; no with CD 4 or CD 8
IL 1 and IL 6
No because no peptide fragment!
Antibody mediated cytotoxicity; either complement dependent or complement independent
13. What is the presentation of Brutons agammaglobulinemia?
False! B cell class switching requires a second signal
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
carboxy terminal
14. What are the mediators that mast cells release?
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Chronic granulomatous disease
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
15. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
IL 1 and IL 6
MHC II - B7
Barrel hoop basement membrane fenestrations
16. Type Iv hypersensitivity is...
delayed!
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Edema and necrosis in that region
17. What are the autoantibodies for wegeners granulomatosis?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
...
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
18. What is thrombopoietin used for?
Thrombocytopenia
Cytokine IL 10 secreted by Th2
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Celiac
19. What are MHC's necessary for? By themselves?
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
T cell activation; no with CD 4 or CD 8
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
20. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Rheumatic arthritis
IgM and IgG
cannot cross placenta
21. What does IL 5 do?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
22. What is the mechanism for sirolimus? what else it known as?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Kill them because they have CD16 on them that recognize the FcG portion
A - B - C; all the D's
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
23. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
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
Popliteal
24. What cytokines to Th2 secrete?
Axillary
Anti U1 RNP (ribonucleoprotein)
In the germinal center of secondary follicles (In the paler center)
IL 4 - 5 - 10 - 6
25. What is the treatment of acute transplant rejection?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IL 1 and IL 6
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
Cyclosporine - OKT3
26. which antibody is involved in the primary response or immediate response to an antigen?
Local infection/inflammation; infection of the ln itself; metastasis
Anti U1 RNP (ribonucleoprotein)
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
IgM
27. Which are the only two antiinflammatory cytokines?
A chemotactic factor for neutrophils
Anti TSh receptor
TGF beta and IL 10
Hemochromatosis
28. Describe complement dependent Type II hypersensitivity. Give an example.
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
Activates Th1 helper cells; Macrophages
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Secretory component
29. What are the autoantibodies for primary biliary cirrhosis?
Axillary
Yes
Anti mitochondrial
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
30. What is the autoantibody for SLE that is nonspecific? Specific?
DM type I
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
31. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
cannot cross placenta
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
32. What are the main cell surface proteins on B cells?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Type IV
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
33. Leukocyte adhesion defect presents with...
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
neutrophilia!
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
34. The alternative pathway is the only constutively...
Anemias (esp due to renal failure)
active complement pathway
Anti Jo -1
NK cells
35. What are the autoantibodies for systemic sclerosis?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Anti topoisomerase
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
36. The ______ in the BM are DN - the DP are in the cortex of thymus
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
type four
Activates Th1 helper cells; Macrophages
T cell precursor
37. What are the PALS?
In the germinal center of secondary follicles (In the paler center)
not Ab mediated
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
38. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Wiskott Aldrich syndrome
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
39. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Carbohydrate
IgM and IgG
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
40. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Rheumatic arthritis
41. What lymph node drains the lateral side of the dorsum of the foot?
Anti alpha subunit 3 of collagen on type IV bm
Carbohydrate
Popliteal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
42. What is immune complex disease? give an example.
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
MHC II - B7
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
43. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
IgG
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
44. What does interferon gamma do to be antiviral?
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
not Ab mediated
Celiac
Increases expression of MHC I and MHC II and also activates NK cells
45. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Axillary
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
46. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
MS - hay fever - SLE - goodpastures
Influenza; antigenic shift; antigenic drift
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
47. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
No because no peptide fragment!
Interferon gamma; Th1
A recomb cytokine of IL 2; RCC and metastatic melanoma
48. What is the marginal zone of the spleen? what happens there?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
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
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
49. IgM can exist as a _______ also
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
pentamer
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immunosuppression after kidney transplantation
50. are Th cells involved in trapping of antigens of endotoxin/LPS?
2 heavy chains and two light chains
MHC class molecules bind to KIRS or CD94 to prevent killing
No because no peptide fragment!
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