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Test your basic knowledge |
USMLE Step 1 Immunology
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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 bacteria are a splenectomy patient most susceptible to? why?
IgM and IgD
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
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
C5a
2. 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?
Basophils! THey want IG E class switch!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
IL 5
3. What does it mean if there are igM in the serum at birth?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
4. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Sinusitis - otitis media - pneumonia
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
5. What are the main Cell surface proteins on T cells?
IgG
When you select for which MHC it will have; take out the lymphs that self react
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
delayed!
6. The MALT/GALT are not...
Its a serine protease that activates apoptosis; NK and CD8
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
C5a
encapsulated
7. What is the main function of IL 12? other than macrophages who else can release IL 12?
Antidote for digoxin intoxication
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
8. What is the toxicity of muromonab?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
T cell dysfunction
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
9. Which are the only two antiinflammatory cytokines?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
C5a
TGF beta and IL 10
10. Which is the most abundant antibody in blood?
Rheumatic arthritis
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
IgG
11. What are the labs in brutons agammaglobulinemia?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Basophils! THey want IG E class switch!
Complement activation (active in both)
12. What do mature naive B lymphocytes express?
Tetanus - Botulinum - HBV - Rabies
IgM and IgD
The igA found in breast milk
IgG
13. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
14. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti Jo -1
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
IgM and IgD
15. which cells have more complete tolerance - B or T cells?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Antidesmoglein
Alternative splicing of mRNA
T
16. Which disease is associated with DR7?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
Steroid responsive nephrotic syndrome
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
17. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti TSh receptor
18. What are howell jolly bodies?
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
A - B - C; all the D's
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
19. Other than stimulating fever - what else does IL 6 do?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IL 5
Stimulate the liver to release acute phase reactants
20. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Cyclosporine - OKT3
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
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
21. The secondary follicles have __________; primary follicles are dense
Graves
Popliteal
A - B - C; all the D's
pale central germinal centers
22. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
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
IgG
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
23. What are the autoantibodies for primary biliary cirrhosis?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Anti mitochondrial
Anemias (esp due to renal failure)
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
24. What is passive immunity?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cyclosporine - OKT3
Receiving preformed Antibodies
TGF beta and IL 10
25. What bugs can actually infect the lymph node itself?
Anti mitochondrial
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Secretory component
26. What is colostrum?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
The igA found in breast milk
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Liver! (they are proteins circulating in the blood)
27. What is the clinical use for azathioprine?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
...
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
28. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
TNF alpha and IL1
Local infection/inflammation; infection of the ln itself; metastasis
29. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgM and IgG
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
30. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Superior mesenteric
Anti smooth muscle
Celiac
31. What are the autoantibodies for systemic sclerosis?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti topoisomerase
32. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
IgM and 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!
33. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Severe pyogenic infections early in life
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Histamine; post capillary venules - vasodilation
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
34. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
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
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
35. Complements are...
acute phase reactants
Anti alpha subunit 3 of collagen on type IV bm
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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!
36. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
TLR ad nuclear receptors
By transcytosis
Cross link
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
37. what mediates the type II hypersensitivity? What are the two different methods?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
Fc
Antibody mediated cytotoxicity; either complement dependent or complement independent
38. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
39. 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)?
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
The patient could become cyanotic in the OR!
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
40. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
A - B - C; all the D's
except hyperacute
MHC II - B7
41. Which type of selection of thymic development provides central tolerance?
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
IgM and IgA
Negative selection
Th2; Th1
42. Which diseases are associated with DR5?
IL 5
Thrombocytopenia
Tetanus - Botulinum - HBV - Rabies
Pernicious Anemia and Hashimotos
43. What are the autoantibodies for pernicious anemia?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Anti IF
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
44. What is the main function of interferons?
No because no peptide fragment!
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
45. What is the main function of IL 8?
Th2; Th1
A chemotactic factor for neutrophils
A recomb cytokine of IL 2; RCC and metastatic melanoma
If there is class switching and plasma cell production (that is when memory cells are produced)
46. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Edema and necrosis in that region
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Wiskott Aldrich syndrome
47. What is muromonab - CD3 (OKT3)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgAs in mothers breast milk!
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
48. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IgE; by activating eosinophils
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgM and IgG
49. Which antibodies can be multimeric?
MHC I; from RER with help of the B2 microglobulin
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Thrombocytopenia
IgM and IgA
50. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Liver! (they are proteins circulating in the blood)
Paracortex
Its main effect is a defect in Ab opsonization for killing