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Test your basic knowledge |
USMLE Step 1 Immunology
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health-sciences
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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 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?
The igA found in breast milk
Histamine; post capillary venules - vasodilation
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
IgAs in mothers breast milk!
2. The lymphocytes are ________ origin
Hereditary angioedema; PNH
mesenchymal
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
3. Which are the only two antiinflammatory cytokines?
NK cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
TGF beta and IL 10
Superior mesenteric
4. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
Barrel hoop basement membrane fenestrations
Activate macrophages
IgG
5. Which cytokines do Th2 release and For what?
type four
active complement pathway
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 :(
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
6. What is the general structure of an Ab?
Recom IL 11; thrombocytopenia
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
lowest concentration
2 heavy chains and two light chains
7. What is recomb beta interferon used for?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
MS
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)
SP infections
8. where are complements produced?
When you select for which MHC it will have; take out the lymphs that self react
MHC I; from RER with help of the B2 microglobulin
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Liver! (they are proteins circulating in the blood)
9. The ______ in the BM are DN - the DP are in the cortex of thymus
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
delayed!
Anti viral and anti tumor
T cell precursor
10. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Axillary
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 :(
Anemias (esp due to renal failure)
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
11. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Negative nitroblue tetrazolium reduction test
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
...
No because no peptide fragment!
12. Which HLA's are included in MHC I? MHC II?
A - B - C; all the D's
type four
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
13. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
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
pale central germinal centers
14. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Negative nitroblue tetrazolium reduction test
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Lymphocytes
15. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Acts as second signal on B cells to induce class switching to IgE and IgG
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Steroid responsive nephrotic syndrome
16. What is the marginal zone of the spleen? what happens there?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
17. which of the transplant rejections is antibody mediated? why does it occur?
active complement pathway
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
TGF beta and IL 10
Macrophages - Dendritic cells - B cells
18. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
19. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Antidote for digoxin intoxication
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
20. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
IgG
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti glutamate carboxylase and anti insulin
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
21. In general What are T cells good for?
IL 4 - 5 - 10 - 6
Anti viral and anti tumor
Negative selection
Superficial inguinal
22. How is the antigen loaded onto a MHC II?
2 heavy chains and two light chains
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
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
23. How does complement link innate and adaptive?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Interferon gamma; Th1
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
24. describe the classic complement pathway.
neutrophilia!
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
25. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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!
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Axillary
26. How fast does it occur?
IL 15; IL 12 - interferon Beta and interferon alpha
Superficial inguinal
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
The patient could become cyanotic in the OR!
27. What lymph node drains the testes?
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
Anti IF
Para aortic
Secretory component
28. In thymic development - What is the positive selection? negative selections?
Celiac
When you select for which MHC it will have; take out the lymphs that self react
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 IF
29. To what disease do the autoantibodies to IgG (rheumatoid factor)?
IgG
Previous transfusion; pregnant woman whose fetus had paternal antigens
Bind FcG for antibody dependent cellular cytotoxicity
Rheumatic arthritis
30. what cell surface marker is used for NK cells as it is unique to them?
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
TGF beta and IL 10
IL 3; supports growth and differentiation of bone marrow stem cells
CD56
31. What are the main cell surface proteins on B cells?
Chronic granulomatous disease
T
Viral neutralization of igM and IgG!
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
32. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Delayed type hypersensitivity
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
33. which antibodies prevent antigens from binding mucosal surfaces?
2 heavy chains and two light chains
IgE; by activating eosinophils
IgA
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
34. what prevents NK cells from killing normal cells if their default is to kill?
Anemias (esp due to renal failure)
MHC class molecules bind to KIRS or CD94 to prevent killing
Anti alpha subunit 3 of collagen on type IV bm
encapsulated
35. 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
No because no peptide fragment!
Antimicrosomal and antithyroglobulin
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
36. Describe the Mannose Lectin pathway
MHC I; from RER with help of the B2 microglobulin
neutrophilia!
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
Pernicious Anemia and Hashimotos
37. IgM can exist as a _______ also
Histamine; post capillary venules - vasodilation
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IL 4 - 5 - 10 - 6
pentamer
38. What lymph node drains the sigmoid colon?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Inferior mesenteric
except hyperacute
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
39. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Cyclosporine - OKT3
IgAs in mothers breast milk!
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
40. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
IL 4 - 5 - 10 - 6
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
T
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
41. What is the main function of IL 8?
T cell dysfunction
except hyperacute
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
A chemotactic factor for neutrophils
42. What is the pathogenesis of acute transplant rejection? When does it occur?
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
43. Which diseases are associated with DR5?
Its main effect is a defect in Ab opsonization for killing
Pernicious Anemia and Hashimotos
IgM and IgA
Remove encapsulated bacateria
44. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
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
Glycoproteins; HLA
45. Describe the capsular structure of a lymph node; What are the functions of the LN?
pathogenesis
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
If there is class switching and plasma cell production (that is when memory cells are produced)
46. when can graft versus host disease? What is the result?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Acts as second signal on B cells to induce class switching to IgE and IgG
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
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
47. What is the white pulp of the spleen?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Complement activation (active in both)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
48. What is the most common example of passive immunity?
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgAs in mothers breast milk!
49. A lymph node is a ________ lymphoid organ.
Popliteal
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
A chemotactic factor for neutrophils
secondary
50. which cytokine inhibits TH2 cells? secreted by who?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Viral neutralization of igM and IgG!
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Interferon gamma; Th1
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