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Test your basic knowledge |
USMLE Step 1 Immunology
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health-sciences
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usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
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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 amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
If there is class switching and plasma cell production (that is when memory cells are produced)
Cyclosporine - OKT3
Histamine; post capillary venules - vasodilation
SP infections
2. What does IL 10 do? who is secreted by?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
3. What is recomb beta interferon used for?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Steroid responsive nephrotic syndrome
MS
Th2; Th1
4. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
Cytokine IL 10 secreted by Th2
T cell precursor
Activate macrophages
5. Type Iv hypersensitivity is...
opsonizes
delayed!
cannot cross placenta
Humoral
6. What is the treatment of acute transplant rejection?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cyclosporine - OKT3
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
7. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
8. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
DM type I and RA
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!
TNF alpha and IL1
9. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Active; passive - fast but short half life (3 weeks!)
Cyclosporine - OKT3
10. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Steroid responsive nephrotic syndrome
except hyperacute
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
11. To what portion of the Antibody do the complements bind?
Fc
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
isotype
12. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Anti U1 RNP (ribonucleoprotein)
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
13. What are the autoantibodies for systemic sclerosis?
No because no peptide fragment!
Fc
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
Anti topoisomerase
14. Which disease is associated with DR3?
DM type I
C5a
By transcytosis
Negative selection
15. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
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!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
pale central germinal centers
Daclizumab; prevent ACUTE rejection of renal transplant
16. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Lymphocytes
dimer
17. ________ regulate the cell mediated response.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
If there is class switching and plasma cell production (that is when memory cells are produced)
Humoral
IgM and IgD
18. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Remove encapsulated bacateria
19. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
The patient could become cyanotic in the OR!
Edema and necrosis in that region
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
pathogenesis
20. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
Lymphocytes
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IL 3; supports growth and differentiation of bone marrow stem cells
21. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Internal iliac
Th cells fail to produce interferon gamma; a lot of IgE
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
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
22. What are the autoantibodies for graves?
Anti TSh receptor
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Paracortex; viral infection
Anti IF
23. IgM can exist as a _______ also
Negative nitroblue tetrazolium reduction test
pentamer
Active; passive - fast but short half life (3 weeks!)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
24. What does IgA pick up from epithelial cells before being secreted?
Lymphocytes
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
Secretory component
MS
25. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
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
26. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
When you select for which MHC it will have; take out the lymphs that self react
Superficial inguinal
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
27. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Its a serine protease that activates apoptosis; NK and CD8
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
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)
28. what will NK cells do to cells covered in IgG Ab? why?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Its a serine protease that activates apoptosis; NK and CD8
Kill them because they have CD16 on them that recognize the FcG portion
Histamine; post capillary venules - vasodilation
29. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
B - T - and NK cells
Antibody mediated cytotoxicity; either complement dependent or complement independent
Active; passive - fast but short half life (3 weeks!)
30. How is the thymus organized? what happens in each section?
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
31. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Its a serine protease that activates apoptosis; NK and CD8
Axillary
32. How is the antigen loaded onto a MHC II?
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
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
NK cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
33. What is the clinical use of Muromonab?
Wiskott Aldrich syndrome
Immunosuppression after kidney transplantation
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
34. What are the autoantibodies for drug induced lupus?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Antihistone
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
35. What is the mechanism for sirolimus? what else it known as?
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
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
All MHC 1/CD8
36. What are the autoantibodies for type I diabetes mellitus?
Complement activation (active in both)
Anti glutamate carboxylase and anti insulin
A chemotactic factor for neutrophils
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
37. What lymph node drains the lateral side of the dorsum of the foot?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Popliteal
Secretory component
In the germinal center of secondary follicles (In the paler center)
38. 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?
Increases expression of MHC I and MHC II and also activates NK cells
B - T - and NK cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
39. The alternative pathway is the only constutively...
active complement pathway
DM type I and RA
pentamer
IgAs in mothers breast milk!
40. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Hereditary angioedema; PNH
Superior mesenteric
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
41. which interleukin receptor is required for NK development? activation?
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
IL 15; IL 12 - interferon Beta and interferon alpha
Lymphocytes
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
42. which B and T cell disorder presents with specifically low IgM?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Wiskott Aldrich syndrome
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Rheumatic arthritis
43. Give an example of someone who could get hyperacute transplant rejection.
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgAs in mothers breast milk!
44. What lymph node drains the breast?
Axillary
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
TLR ad nuclear receptors
45. What lymph node drains the thigh?
IgG
Superficial inguinal
Cytokine IL 10 secreted by Th2
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
46. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Immunosuppression after kidney transplantation
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
47. What are C1 - C2 - C3 - C4 important for?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Viral neutralization of igM and IgG!
Yes
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
48. What are the autoantibodies for primary biliary cirrhosis?
MHC I; from RER with help of the B2 microglobulin
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti mitochondrial
Anti TSh receptor
49. which of the hypersensitivity reactions is not Ab mediated?
Anti topoisomerase
pentamer
Type IV
Macrophages - Dendritic cells - B cells
50. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
If there is class switching and plasma cell production (that is when memory cells are produced)
Sinusitis - otitis media - pneumonia
pathogenesis
Sorry!:) No result found.
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