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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. IgM can fix complement but...
cannot cross placenta
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgAs in mothers breast milk!
Type IV
2. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
Its a serine protease that activates apoptosis; NK and CD8
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 3; supports growth and differentiation of bone marrow stem cells
3. which of the hypersensitivity reactions is not Ab mediated?
Humoral
Type IV
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
By transcytosis
4. Which disease is associated withB B27?
DM type I
Lymphocytes
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
5. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
The igA found in breast milk
active complement pathway
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
6. Leukocyte adhesion defect presents with...
Wiskott Aldrich syndrome
neutrophilia!
TGF beta and IL 10
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
7. which antibody activate mast cells - basophils - and eosinophils?
Superficial inguinal
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgE
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
8. What are the main symptoms of B cell immunodeficiencies?
TGF beta and IL 10
SP infections
IgM
Anti topoisomerase
9. What are the mediators that mast cells release?
Sinusitis - otitis media - pneumonia
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
10. Which is the most abundant antibody in blood?
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Anti glutamate carboxylase and anti insulin
IgG
11. What are the T cell functions?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Stimulate the liver to release acute phase reactants
12. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
pale central germinal centers
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
13. What does IgA pick up from epithelial cells before being secreted?
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
Secretory component
Cyclosporine - OKT3
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
14. give an example of how influenza does a major antigenic shift.
MHC I - CD16 - CD56
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
RNA segment reassortment
isotype
15. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
IL 4 - 5 - 10 - 6
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
16. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
secondary
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
17. What is the white pulp of the spleen?
IL 4 - 5 - 10 - 6
Secretory component
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
lowest concentration
18. What is a type I hypersensitivity reaction? What is atopic?
T
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
19. What is anergy? why does this occur?
Negative nitroblue tetrazolium reduction test
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
B - T - and NK cells
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
20. What lymph node drains the breast?
Alternative splicing of mRNA
IgA
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Axillary
21. What are the autoantibodies for pemphigus bulgaris?
IgG
Bind FcG for antibody dependent cellular cytotoxicity
Antidesmoglein
Complement activation (active in both)
22. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Antidesmoglein
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
23. What is the most common example of passive immunity?
Steroid responsive nephrotic syndrome
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
MHC II - B7
IgAs in mothers breast milk!
24. What is oprelevkin? and What is it used for?
IL 5
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
Recom IL 11; thrombocytopenia
opsonizes
25. How do you test for type III hypersensitivity?
Antibody mediated cytotoxicity; either complement dependent or complement independent
NK cells
secondary
Immunoflourescent staining of tissue biopsies
26. What is a factor that is a predictor for a bad transplantation?
Glycoproteins; HLA
MS - hay fever - SLE - goodpastures
The patient could become cyanotic in the OR!
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
27. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Yes
Sinusitis - otitis media - pneumonia
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
IgA
28. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
DM type I
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
Fc
29. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Sinusitis - otitis media - pneumonia
Anti topoisomerase
isotype
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
30. Give an example of someone who could get hyperacute transplant rejection.
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
...
Previous transfusion; pregnant woman whose fetus had paternal antigens
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
31. Which is the main antibody that provides passive immunity to infants?
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
IgG
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
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
32. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IgM
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
33. what happens in a deficiency of C1 esterase inhibitor? DAF?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Remove encapsulated bacateria
Hereditary angioedema; PNH
T cell dysfunction
34. What lymph node drains the upper limb?
TNF alpha and IL1
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Remove encapsulated bacateria
Axillary
35. Which is the main antibody in the delayed or secondary response to an antigen?
CRP - C3b - IgM
IgG
Paracortex
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
36. What are the autoantibodies for myasthenia gravis?
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
Daclizumab; prevent ACUTE rejection of renal transplant
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti Ach receptor
37. Complements are...
acute phase reactants
lowest concentration
S. aureus - E. Coli - aspergillus
Hemochromatosis
38. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
Influenza; antigenic shift; antigenic drift
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
opsonizes
39. What are the two signals to kill for NK cells?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
isotype
Popliteal
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
40. How is the thymus organized? what happens in each section?
encapsulated
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
41. which interleukin receptor is required for NK development? activation?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IL 15; IL 12 - interferon Beta and interferon alpha
Steroid responsive nephrotic syndrome
Cross link
42. How is i Th1 helper cell inhibited?
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
Cytokine IL 10 secreted by Th2
A chemotactic factor for neutrophils
Activates Th1 helper cells; Macrophages
43. 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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Anti alpha subunit 3 of collagen on type IV bm
Not thymus - BM
44. What are the autoantibodies for graves?
Anti TSh receptor
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
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 and IgD
45. is IgM an opsonizer?
Negative!
Sinusitis - otitis media - pneumonia
CRP - C3b - IgM
Anti U1 RNP (ribonucleoprotein)
46. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
47. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Kill them because they have CD16 on them that recognize the FcG portion
Cells that stil have weird parts of their membrane that macrophages usually bite off
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
48. Which MHC presents intracellular peptides? how so?
MHC I; from RER with help of the B2 microglobulin
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
TNF alpha and IL1
49. what mediates the type II hypersensitivity? What are the two different methods?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IL 3; supports growth and differentiation of bone marrow stem cells
Antibody mediated cytotoxicity; either complement dependent or complement independent
50. describe the pathogenesis of delayed type IV hypersensitivity
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
Remove encapsulated bacateria
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anti smooth muscle