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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
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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. Which antibody mediates immunity to worms? how?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgE; by activating eosinophils
2. ________ regulate the cell mediated response.
mesenchymal
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Paracortex
Humoral
3. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
No because no peptide fragment!
By transcytosis
4. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Axillary
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
5. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
T cell precursor
Severe pyogenic infections early in life
6. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
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
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)
7. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Basophils! THey want IG E class switch!
8. What is an example of a parasite showing antigenic variation?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cyclosporine - OKT3
9. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
lowest concentration
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Paracortex
10. which antibodies can bind complement?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
IgA
Antidote for digoxin intoxication
IgM and IgG
11. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
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
12. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
cannot cross placenta
Thrombocytopenia
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
Severe pyogenic infections early in life
13. what cytokine does basophils secrete?
IL 4
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
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
pale central germinal centers
14. Which diseases are associated with DR4?
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
MHC I; from RER with help of the B2 microglobulin
DM type I and RA
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
15. Which is the main antibody that provides passive immunity to infants?
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
IgG
Hereditary angioedema; PNH
Pernicious Anemia and Hashimotos
16. What happens in a secondary follicle?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Th cells fail to produce interferon gamma; a lot of IgE
17. What are the autoantibodies for goodpastures syndrome?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Its a serine protease that activates apoptosis; NK and CD8
Anti alpha subunit 3 of collagen on type IV bm
Kill them because they have CD16 on them that recognize the FcG portion
18. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 4 - 5 - 10 - 6
...
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
19. The secondary follicles have __________; primary follicles are dense
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
T cell precursor
Complement activation (active in both)
pale central germinal centers
20. T/F B cells do not require a second signal
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anemias (esp due to renal failure)
False! B cell class switching requires a second signal
21. What are the autoantibodies for pemphigus bulgaris?
Humoral
Antidesmoglein
Its main effect is a defect in Ab opsonization for killing
Anti viral and anti tumor
22. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
cannot cross placenta
Inferior mesenteric
MS - hay fever - SLE - goodpastures
23. What is the clinical use for azathioprine?
Immunoflourescent staining of tissue biopsies
Influenza; antigenic shift; antigenic drift
...
Anti alpha subunit 3 of collagen on type IV bm
24. is IgM an opsonizer?
The patient could become cyanotic in the OR!
Negative!
IgM and IgD
IgE; by activating eosinophils
25. which type of immunity is slow but long lasting? as opposed to...
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
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
IgA
Active; passive - fast but short half life (3 weeks!)
26. What are the autoantibodies for pernicious anemia?
Thrombocytopenia
Anti IF
Secretory component
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
27. What is chronic mucocutaneous candidiasis d/t?
encapsulated
T cell dysfunction
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
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
28. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
A chemotactic factor for neutrophils
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
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)
Fab portion
29. What is serum sickness? give an example.
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
SP infections
30. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Antidesmoglein
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
MS - hay fever - SLE - goodpastures
Secretory component
31. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
MS
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
32. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
33. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
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
Tetanus - Botulinum - HBV - Rabies
34. Type Iv hypersensitivity is...
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Humoral
delayed!
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
35. How does the alternative pathway lead to MAC activation?
encapsulated
IgM
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
36. The two heavy chains of an antibody contribute to the...
Anti Ach receptor
Fab portion
Superficial inguinal
IL 1 and IL 6
37. What are the three types of lymphocytes?
Remove encapsulated bacateria
B - T - and NK cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
except hyperacute
38. What are the PALS?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
MS - hay fever - SLE - goodpastures
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
39. The lymphocytes are ________ origin
Negative!
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
mesenchymal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
40. Which HLA's are included in MHC I? MHC II?
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41. What is the pathology of acute transplant rejection? is it reversible?
A chemotactic factor for neutrophils
MHC I - CD16 - CD56
Complement activation (active in both)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
42. What are some sinopulmonary infections?
SP infections
Sinusitis - otitis media - pneumonia
Yes
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
43. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
IgG
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
CD56
T cell precursor
44. IgE has the ___________ in the serum
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
carboxy terminal
lowest concentration
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
45. What is the receptor for EBV? On what cells is that located?
Alternative splicing of mRNA
Anti Jo -1
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IL 5
46. What is epo used for?
Anemias (esp due to renal failure)
Alternative splicing of mRNA
No because no peptide fragment!
IgA
47. The idiotype; the Fc portion determines the...
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
isotype
A - B - C; all the D's
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
48. What do mature naive B lymphocytes express?
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IgM and IgD
Activates Th1 helper cells; Macrophages
49. Complements are...
pathogenesis
IgG
acute phase reactants
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
50. which cells have more complete tolerance - B or T cells?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Negative selection
T
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)