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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. What lymph node drains the thigh?
Superficial inguinal
Cross link
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
2. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Inferior mesenteric
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Thrombocytopenia
3. What are the T cell functions?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
mesenchymal
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
4. What is filgrastim and sargramostim? and What is it used for?
Immunosuppression after kidney transplantation
Immunoflourescent staining of tissue biopsies
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
5. Which antibody mediates immunity to worms? how?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Superficial inguinal
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgE; by activating eosinophils
6. What is the treatment of acute transplant rejection?
Viral neutralization of igM and IgG!
Negative!
Axillary
Cyclosporine - OKT3
7. Which disease is associated with DR3?
DM type I
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 :(
T cell dysfunction
All MHC 1/CD8
8. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
mesenchymal
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Axillary
9. Which is the main antibody that provides passive immunity to infants?
IgG
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
opsonizes
Popliteal
10. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
isotype
Local infection/inflammation; infection of the ln itself; metastasis
Anti Jo -1
11. What kinds of receptors activate innate immunity?
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
TLR ad nuclear receptors
Cross link
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
12. Complements are...
acute phase reactants
IL 4 - 5 - 10 - 6
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
Interferon gamma; Th1
13. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Paracortex; viral infection
14. What can cause a lymph node enlargement?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Local infection/inflammation; infection of the ln itself; metastasis
A recomb cytokine of IL 2; RCC and metastatic melanoma
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
15. 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?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
T
16. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Internal iliac
All MHC 1/CD8
No because no peptide fragment!
17. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
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
Popliteal
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
18. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Humoral
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
19. What is the pathogenesis of a candida skin test?
Graves
Delayed type hypersensitivity
In the germinal center of secondary follicles (In the paler center)
not Ab mediated
20. Which type of selection of thymic development provides central tolerance?
TGF beta and IL 10
Negative selection
secondary
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
21. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
IgAs in mothers breast milk!
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
By transcytosis
22. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
Anti glutamate carboxylase and anti insulin
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Hemochromatosis
23. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Daclizumab; prevent ACUTE rejection of renal transplant
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
24. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
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
IgE; by activating eosinophils
MS
25. 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
Negative!
Th cells fail to produce interferon gamma; a lot of IgE
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
26. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
pale central germinal centers
Popliteal
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
27. The alternative pathway is the only constutively...
Recom IL 11; thrombocytopenia
active complement pathway
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
RNA segment reassortment
28. How do you test for chronic granulomatous disease?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Negative nitroblue tetrazolium reduction test
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
MS
29. Which diseases are associated with DR5?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Pernicious Anemia and Hashimotos
MHC II - B7
Humoral
30. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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!
Anti Jo -1
31. What bugs can actually infect the lymph node itself?
Anti SS- A (anti RO) and Anti SS- B
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
A chemotactic factor for neutrophils
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
32. T/F B cells do not require a second signal
Axillary
The igA found in breast milk
False! B cell class switching requires a second signal
Paracortex; viral infection
33. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti SS- A (anti RO) and Anti SS- B
Th2; Th1
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!
34. For which toxins are preformed antibodies (passive) given?
Superficial inguinal
Tetanus - Botulinum - HBV - Rabies
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!
lowest concentration
35. What are the autoantibodies for wegeners granulomatosis?
Inferior mesenteric
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgE
36. Name the three opsonins
Negative!
Bind FcG for antibody dependent cellular cytotoxicity
Th cells fail to produce interferon gamma; a lot of IgE
CRP - C3b - IgM
37. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Daclizumab; prevent ACUTE rejection of renal transplant
Antibody mediated cytotoxicity; either complement dependent or complement independent
Immunoflourescent staining of tissue biopsies
38. What does IL 4 do?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
not Ab mediated
Acts as second signal on B cells to induce class switching to IgE and IgG
2 heavy chains and two light chains
39. The pathogenesis of contact dermatitis is ________ hypersensitivity
Immunoflourescent staining of tissue biopsies
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
type four
40. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Secretory component
Hereditary angioedema; PNH
41. 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
Glycoproteins; HLA
IgE; by activating eosinophils
Its main effect is a defect in Ab opsonization for killing
42. What are the autoantibodies for other vasculitides?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
43. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Anti smooth muscle
Its main effect is a defect in Ab opsonization for killing
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
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
44. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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!
T
Axillary
45. The MALT/GALT are not...
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
encapsulated
Anti glutamate carboxylase and anti insulin
46. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Local infection/inflammation; infection of the ln itself; metastasis
Anti alpha subunit 3 of collagen on type IV bm
Glycoproteins; HLA
47. What lymph node drains the rectum (above the pectinate line)?
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
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!
Negative!
Internal iliac
48. are Th cells involved in trapping of antigens of endotoxin/LPS?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
No because no peptide fragment!
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
pale central germinal centers
49. What does IgA pick up from epithelial cells before being secreted?
Interferon gamma and IL 2
Secretory component
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
50. What is muromonab - CD3 (OKT3)
S. aureus - E. Coli - aspergillus
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
MHC I; from RER with help of the B2 microglobulin
T cells react to the angtigen and activate leukocyted (macrophage acitivation)