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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. where do somatic hypermutation and class switching occur?
...
IgM and IgA
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
In the germinal center of secondary follicles (In the paler center)
2. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
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
A j chain
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
3. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Liver! (they are proteins circulating in the blood)
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
IL 5
4. What happens in a deficiency of C3?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
A j chain
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
5. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Antihistone
Influenza; antigenic shift; antigenic drift
Activate macrophages
Thrombocytopenia
6. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Hemochromatosis
Yes
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
7. What are the labs in brutons agammaglobulinemia?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
TLR ad nuclear receptors
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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. What does IL 2 do?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Activates cytotoxic CD 8 T cells as second signal
Alternative splicing of mRNA
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
9. What cytokines to Th2 secrete?
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
IL 4 - 5 - 10 - 6
Hemochromatosis
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
10. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Cross link
Anti mitochondrial
11. What are the main cell surface proteins on B cells?
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Thrombocytopenia
12. What type of side chains are found on Fc region of an antibody?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Carbohydrate
Steroid responsive nephrotic syndrome
Complement activation (active in both)
13. What is an example of a parasite showing antigenic variation?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgG
14. How do you test for chronic granulomatous disease?
Active; passive - fast but short half life (3 weeks!)
Anti glutamate carboxylase and anti insulin
Negative nitroblue tetrazolium reduction test
Axillary
15. IgM can fix complement but...
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
encapsulated
cannot cross placenta
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
16. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
17. Complements are...
acute phase reactants
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgE
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
18. What is the mechanism for sirolimus? what else it known as?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
Antimicrosomal and antithyroglobulin
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
19. In general What are T cells good for?
Superficial inguinal
Anti viral and anti tumor
type four
Anti U1 RNP (ribonucleoprotein)
20. what prevents NK cells from killing normal cells if their default is to kill?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antidote for digoxin intoxication
MHC class molecules bind to KIRS or CD94 to prevent killing
Wiskott Aldrich syndrome
21. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
C5a
TNF alpha and IL1
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
TLR ad nuclear receptors
22. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Fc
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anti Jo -1
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
23. Which disease is associated with HLA A3?
Hemochromatosis
S. aureus - E. Coli - aspergillus
Viral neutralization of igM and IgG!
Anti U1 RNP (ribonucleoprotein)
24. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Anemias (esp due to renal failure)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
No because no peptide fragment!
25. The alternative pathway is the only constutively...
Interferon gamma; Th1
Anti SS- A (anti RO) and Anti SS- B
active complement pathway
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
26. What are the two signals required for B cell class switching? Which is the second signal?
B - T - and NK cells
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Axillary
27. The MALT/GALT are not...
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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)
encapsulated
28. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
Superficial inguinal
MHC class molecules bind to KIRS or CD94 to prevent killing
Th cells fail to produce interferon gamma; a lot of IgE
29. What are the PALS?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
delayed!
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
30. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Antibody mediated cytotoxicity; either complement dependent or complement independent
31. What are the main symptoms of B cell immunodeficiencies?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Carbohydrate
SP infections
RNA segment reassortment
32. What lymph node drains the breast?
Thrombocytopenia
The patient could become cyanotic in the OR!
Th2; Th1
Axillary
33. What lymph node drains the rectum (above the pectinate line)?
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
A - B - C; all the D's
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Internal iliac
34. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
secondary
Hereditary angioedema; PNH
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Anti mitochondrial
MHC II - B7
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
36. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
37. What lymph node drains the thigh?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Superficial inguinal
38. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Delayed type hypersensitivity
IgG
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
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
39. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
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
Barrel hoop basement membrane fenestrations
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
40. What is the marginal zone of the spleen? what happens there?
CD56
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
Daclizumab; prevent ACUTE rejection of renal transplant
Antidesmoglein
41. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
carboxy terminal
Steroid responsive nephrotic syndrome
42. 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?
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
Superficial inguinal
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
43. What does IL 10 do? who is secreted by?
Negative!
Activates Th1 helper cells; Macrophages
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
44. How do you test for type III hypersensitivity?
Delayed type hypersensitivity
Immunoflourescent staining of tissue biopsies
...
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
45. Which helper T cells' development is induced by IL 4? IL 12?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Local infection/inflammation; infection of the ln itself; metastasis
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Th2; Th1
46. What are the function of B cells?
Superficial inguinal
opsonizes
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
47. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
IgE
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Glycoproteins; HLA
Complement activation (active in both)
48. What do multimeric antibodies require for assembly?
Receiving preformed Antibodies
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
A j chain
Activate macrophages
49. What does Interferon alpha and beta do? how?
IL 4
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
50. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Fab portion
opsonizes
acute phase reactants