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. What is an example of a parasite showing antigenic variation?
Anti U1 RNP (ribonucleoprotein)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
2. What is the presentation of Brutons agammaglobulinemia?
IgE; by activating eosinophils
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
3. can igG cross the placenta?
Anti SS- A (anti RO) and Anti SS- B
Cyclosporine - OKT3
Yes
Inferior mesenteric
4. What is three common causes of severe combined immunodef? What is the result of all three?
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Negative selection
5. From where do cytokines come from?
Rheumatic arthritis
Anti topoisomerase
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Lymphocytes
6. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Anti mitochondrial
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
Its main effect is a defect in Ab opsonization for killing
7. Which disease is associated with DR7?
Humoral
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antimicrosomal and antithyroglobulin
Steroid responsive nephrotic syndrome
8. What are the PALS?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
lowest concentration
Macrophages - Dendritic cells - B cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
9. What is colostrum?
Viral neutralization of igM and IgG!
...
The igA found in breast milk
IgM
10. What is the receptor for EBV? On what cells is that located?
Antibody mediated cytotoxicity; either complement dependent or complement independent
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
CD21 on B cells (although there is T cell lymphocytosis in EBV)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
11. What are the autoantibodies for graves?
Anti TSh receptor
False! B cell class switching requires a second signal
carboxy terminal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
12. What are some catalase positive organisms?
Recom IL 11; thrombocytopenia
S. aureus - E. Coli - aspergillus
Local infection/inflammation; infection of the ln itself; metastasis
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
13. Which disease is associated with B8?
Basophils! THey want IG E class switch!
isotype
Graves
Macrophages - Dendritic cells - B cells
14. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Humoral
TLR ad nuclear receptors
15. What are howell jolly bodies?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
pentamer
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
16. What is oprelevkin? and What is it used for?
Tetanus - Botulinum - HBV - Rabies
Anti alpha subunit 3 of collagen on type IV bm
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
Recom IL 11; thrombocytopenia
17. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
...
S. aureus - E. Coli - aspergillus
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
18. The pathogenesis of contact dermatitis is ________ hypersensitivity
Acts as second signal on B cells to induce class switching to IgE and IgG
type four
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
19. How is sirolimus different from tacrolimus?
...
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
20. ________ regulate the cell mediated response.
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Severe pyogenic infections early in life
MHC II - B7
Humoral
21. What is immune complex disease? give an example.
Internal iliac
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
active complement pathway
TNF alpha and IL1
22. In thymic development - What is the positive selection? negative selections?
Internal iliac
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Acts as second signal on B cells to induce class switching to IgE and IgG
When you select for which MHC it will have; take out the lymphs that self react
23. describe the classic complement pathway.
Negative nitroblue tetrazolium reduction test
Lymphocytes
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
24. describe the pathogenesis of delayed type IV hypersensitivity
Thrombocytopenia
MS
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
25. What is the pathology seen in chronic transplant rejection?
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
Superficial inguinal
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
26. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
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
pale central germinal centers
Anti TSh receptor
27. Name two endogenous pyrogens
IgE
IL 1 and IL 6
pale central germinal centers
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
28. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
CRP - C3b - IgM
Type IV
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
29. What is a factor that is a predictor for a bad transplantation?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Anti alpha subunit 3 of collagen on type IV bm
30. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
lowest concentration
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
31. which antibodies can bind complement?
NK cells
Complement activation (active in both)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgM and IgG
32. Name 5 ways Antibody diversity is generated?
Activate macrophages
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
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!
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
33. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antibody mediated cytotoxicity; either complement dependent or complement independent
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Cells that stil have weird parts of their membrane that macrophages usually bite off
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?
TGF beta and IL 10
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
35. Type Iv hypersensitivity is...
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Fc
delayed!
When you select for which MHC it will have; take out the lymphs that self react
36. What does IL 2 do?
Antihistone
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Activates cytotoxic CD 8 T cells as second signal
Anti SS- A (anti RO) and Anti SS- B
37. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IgM and IgG
Receiving preformed Antibodies
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IL 15; IL 12 - interferon Beta and interferon alpha
38. What are the autoantibodies for pemphigus bulgaris?
The igA found in breast milk
Celiac
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Antidesmoglein
39. IgG...
Lymphocytes
opsonizes
Active; passive - fast but short half life (3 weeks!)
Remove encapsulated bacateria
40. Monomer in circulation - ___ when secreted
...
dimer
Acts as second signal on B cells to induce class switching to IgE and IgG
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
41. What are the main cell surface proteins on B cells?
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
type four
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
42. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
T cell activation; no with CD 4 or CD 8
Activate macrophages
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. What are the autoantibodies for sjorgens syndrome?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti SS- A (anti RO) and Anti SS- B
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 :(
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
44. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
TLR ad nuclear receptors
Hereditary angioedema; PNH
Graves
45. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Anti alpha subunit 3 of collagen on type IV bm
Antibody mediated cytotoxicity; either complement dependent or complement independent
46. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
IL 4
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Superior mesenteric
Glycoproteins; HLA
47. What are the two signals to kill for NK cells?
opsonizes
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
48. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
active complement pathway
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
IgM
49. What is passive immunity?
lowest concentration
Receiving preformed Antibodies
When you select for which MHC it will have; take out the lymphs that self react
MHC I - CD16 - CD56
50. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
TLR ad nuclear receptors