SUBJECTS
|
BROWSE
|
CAREER CENTER
|
POPULAR
|
JOIN
|
LOGIN
Business Skills
|
Soft Skills
|
Basic Literacy
|
Certifications
About
|
Help
|
Privacy
|
Terms
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. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
...
except hyperacute
SP infections
2. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC I; from RER with help of the B2 microglobulin
Alternative splicing of mRNA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
3. What are the two signals required for T cells? what happens after?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IL 4
Anti smooth muscle
4. Which MHC presents intracellular peptides? how so?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
MHC I; from RER with help of the B2 microglobulin
Cross link
5. What are the labs in brutons agammaglobulinemia?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Influenza; antigenic shift; antigenic drift
Anti U1 RNP (ribonucleoprotein)
6. The idiotype; the Fc portion determines the...
Anti SS- A (anti RO) and Anti SS- B
isotype
In the germinal center of secondary follicles (In the paler center)
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
7. which type of immunity is slow but long lasting? as opposed to...
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Active; passive - fast but short half life (3 weeks!)
Interferon gamma and IL 2
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
8. which antibodies can bind complement?
MHC class molecules bind to KIRS or CD94 to prevent killing
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgM and IgG
Barrel hoop basement membrane fenestrations
9. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
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
Glycoproteins; HLA
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Edema and necrosis in that region
10. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
IgE; by activating eosinophils
Negative nitroblue tetrazolium reduction test
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
11. What is the pathogenesis of a hypersensitivity reaction?
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
B - T - and NK cells
12. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
lowest concentration
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
RNA segment reassortment
13. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
Superior mesenteric
The patient could become cyanotic in the OR!
Superficial inguinal
14. What are the autoantibodies for hashimotos?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Complement activation (active in both)
Antimicrosomal and antithyroglobulin
SP infections
15. Which disease is associated with HLA A3?
Type IV
Chronic granulomatous disease
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
Hemochromatosis
16. Which disease is associated with B8?
IgM and IgG
dimer
Graves
...
17. ________ regulate the cell mediated response.
Humoral
lowest concentration
Th cells fail to produce interferon gamma; a lot of IgE
All MHC 1/CD8
18. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Internal iliac
A j chain
B - T - and NK cells
19. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
20. Name two endogenous pyrogens
Its a serine protease that activates apoptosis; NK and CD8
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IL 1 and IL 6
Anti topoisomerase
21. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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 Ach receptor
22. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
IL 1 and IL 6
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
CD21 on B cells (although there is T cell lymphocytosis in EBV)
23. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
IL 4 - 5 - 10 - 6
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Antidote for digoxin intoxication
Celiac
24. What is the pathogenesis of a candida skin test?
Negative!
Pernicious Anemia and Hashimotos
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
Delayed type hypersensitivity
25. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
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
isotype
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
26. What is oprelevkin? and What is it used for?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Recom IL 11; thrombocytopenia
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Severe pyogenic infections early in life
27. Which helper T cells' development is induced by IL 4? IL 12?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Th2; Th1
28. What are the autoantibodies for primary biliary cirrhosis?
Its main effect is a defect in Ab opsonization for killing
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Anti mitochondrial
29. What cytokines are released by Th1 cells?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
The patient could become cyanotic in the OR!
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Interferon gamma and IL 2
30. What are the autoantibodies for systemic sclerosis?
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
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti topoisomerase
31. What are the two signals required for Th1 cells? what happens after then activated?
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Cells that stil have weird parts of their membrane that macrophages usually bite off
32. In general What are T cells good for?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti topoisomerase
Anti viral and anti tumor
Daclizumab; prevent ACUTE rejection of renal transplant
33. What is the toxicity of azathioprine?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
...
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
acute phase reactants
34. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Histamine; post capillary venules - vasodilation
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IgM and IgG
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
35. Which is the main antibody that provides passive immunity to infants?
IgG
Local infection/inflammation; infection of the ln itself; metastasis
A chemotactic factor for neutrophils
Superior mesenteric
36. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Macrophages - Dendritic cells - B cells
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
37. The secondary follicles have __________; primary follicles are dense
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
pale central germinal centers
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
38. are Th cells involved in trapping of antigens of endotoxin/LPS?
Yes
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
No because no peptide fragment!
39. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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
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
Fc
40. What is the toxicity of muromonab?
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Immunosuppression after kidney transplantation
IgM
41. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
cannot cross placenta
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
encapsulated
42. Which diseases are associated with DR5?
Daclizumab; prevent ACUTE rejection of renal transplant
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Pernicious Anemia and Hashimotos
43. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
44. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
45. What is chronic mucocutaneous candidiasis d/t?
IgM and IgG
T cell dysfunction
Activates Th1 helper cells; 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
46. The ______ in the BM are DN - the DP are in the cortex of thymus
Hemochromatosis
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
T cell precursor
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
47. 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
Pernicious Anemia and Hashimotos
A - B - C; all the D's
MS - hay fever - SLE - goodpastures
48. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Remove encapsulated bacateria
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Previous transfusion; pregnant woman whose fetus had paternal antigens
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
49. What are the mediators that mast cells release?
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
Anti TSh receptor
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
A recomb cytokine of IL 2; RCC and metastatic melanoma
50. Describe the Mannose Lectin pathway
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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