SUBJECTS
|
BROWSE
|
CAREER CENTER
|
POPULAR
|
JOIN
|
LOGIN
Business Skills
|
Soft Skills
|
Basic Literacy
|
Certifications
About
|
Help
|
Privacy
|
Terms
|
Email
Search
Test your basic knowledge |
USMLE Step 1 Immunology
Start Test
Study First
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. Give an example of someone who could get hyperacute transplant rejection.
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
2. IgM can fix complement but...
Th2; Th1
Para aortic
cannot cross placenta
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
3. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Negative selection
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Daclizumab; prevent ACUTE rejection of renal transplant
4. describe the classic complement pathway.
IgM and IgA
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Daclizumab; prevent ACUTE rejection of renal transplant
5. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Interferon gamma and IL 2
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cyclosporine - OKT3
except hyperacute
6. The two heavy chains of an antibody contribute to the...
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Fab portion
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Increases expression of MHC I and MHC II and also activates NK cells
7. What is the marginal zone of the spleen? what happens there?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
8. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
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
Lymphocytes
IgG
9. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Superficial inguinal
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
10. What is the presentation of Brutons agammaglobulinemia?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Recom IL 11; thrombocytopenia
IgM and IgG
11. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
pale central germinal centers
12. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Delayed type hypersensitivity
isotype
Alternative splicing of mRNA
Paracortex; viral infection
13. What lymph node drains the breast?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Stimulate the liver to release acute phase reactants
Axillary
14. What are the cell surface proteins for Macrophages? which two are for opsonins?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
SP infections
Previous transfusion; pregnant woman whose fetus had paternal antigens
15. What is the main cytokine released by T cells? What does it do
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 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 3; supports growth and differentiation of bone marrow stem cells
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
16. What lymph node drains the lateral side of the dorsum of the foot?
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 :(
Graves
Basophils! THey want IG E class switch!
Popliteal
17. what cell surface proteins are on all APCs?
Axillary
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
MHC II - B7
18. What is the pathogenesis of a hypersensitivity reaction?
RNA segment reassortment
CD56
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
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
19. What are the main Cell surface proteins on T cells?
active complement pathway
Activates cytotoxic CD 8 T cells as second signal
IgM and IgD
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
20. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Anti Jo -1
21. What is recomb alpha interferon used for?
Macrophages - Dendritic cells - B cells
Immunosuppression after kidney transplantation
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
The igA found in breast milk
22. Which diseases are associated with DR4?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
DM type I and RA
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti Jo -1
23. what prevents NK cells from killing normal cells if their default is to kill?
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
MHC class molecules bind to KIRS or CD94 to prevent killing
T cell precursor
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
24. What is the pathology of acute transplant rejection? is it reversible?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Fab portion
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
25. which cells have more complete tolerance - B or T cells?
T
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Immunosuppression after kidney transplantation
Its main effect is a defect in Ab opsonization for killing
26. What is the presentation of hyperIgM syndrome?
CD56
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Glycoproteins; HLA
Severe pyogenic infections early in life
27. is IgM an opsonizer?
Axillary
Antimicrosomal and antithyroglobulin
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
Negative!
28. 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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti topoisomerase
29. What does granzyme do? who secretes it?
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
Its a serine protease that activates apoptosis; NK and CD8
Internal iliac
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
30. In general What are T cells good for?
Anti viral and anti tumor
Anti topoisomerase
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Superficial inguinal
31. Which HLA's are included in MHC I? MHC II?
Warning
: Invalid argument supplied for foreach() in
/var/www/html/basicversity.com/show_quiz.php
on line
183
32. What is serum sickness? give an example.
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
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
Complement activation (active in both)
33. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Daclizumab; prevent ACUTE rejection of renal transplant
Its main effect is a defect in Ab opsonization for killing
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
34. What is the pathology in hyperacute transplant rejection?
Receiving preformed Antibodies
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
CRP - C3b - IgM
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
35. What does granulysin do?
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Bind FcG for antibody dependent cellular cytotoxicity
36. A lymph node is a ________ lymphoid organ.
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
secondary
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
37. To what portion of the Antibody do the complements bind?
Anti alpha subunit 3 of collagen on type IV bm
IgE; by activating eosinophils
Not thymus - BM
Fc
38. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Humoral
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
...
39. 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)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
TLR ad nuclear receptors
2 heavy chains and two light chains
40. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
41. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anemias (esp due to renal failure)
Basophils! THey want IG E class switch!
42. Which MHC presents intracellular peptides? how so?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
isotype
MHC I; from RER with help of the B2 microglobulin
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
43. which of the transplant rejections is antibody mediated? why does it occur?
Anti Ach receptor
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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)
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
44. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Activates Th1 helper cells; Macrophages
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MS
CRP - C3b - IgM
45. What is digoxin immune Fab used for?
IgG
Anti TSh receptor
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
Antidote for digoxin intoxication
46. Which disease is associated withB B27?
In the germinal center of secondary follicles (In the paler center)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
DM type I and RA
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
47. where do NK cells develop?
False! B cell class switching requires a second signal
Not thymus - BM
lowest concentration
T cell precursor
48. Which is the main antibody that provides passive immunity to infants?
IgG
IgAs in mothers breast milk!
Th2; Th1
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
49. which type of immunity is slow but long lasting? as opposed to...
IgE
Paracortex
IgG
Active; passive - fast but short half life (3 weeks!)
50. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
isotype
Liver! (they are proteins circulating in the blood)