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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.
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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 exist as a _______ also
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
pentamer
2. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Increases expression of MHC I and MHC II and also activates NK cells
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; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Acts as second signal on B cells to induce class switching to IgE and IgG
3. What does IL 4 do?
IgM and IgA
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Previous transfusion; pregnant woman whose fetus had paternal antigens
Acts as second signal on B cells to induce class switching to IgE and IgG
4. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Receiving preformed Antibodies
mesenchymal
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
5. In thymic development - What is the positive selection? negative selections?
Anti alpha subunit 3 of collagen on type IV bm
When you select for which MHC it will have; take out the lymphs that self react
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
MHC I; from RER with help of the B2 microglobulin
6. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
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
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
7. What are the autoantibodies for pernicious anemia?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Antidote for digoxin intoxication
Th cells fail to produce interferon gamma; a lot of IgE
Anti IF
8. What are the autoantibodies for polymyositis and dermatomyositis?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Yes
Anti Jo -1
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
9. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Activates Th1 helper cells; Macrophages
10. What is passive immunity?
Receiving preformed Antibodies
Cyclosporine - OKT3
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Th cells fail to produce interferon gamma; a lot of IgE
11. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
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
MHC II - B7
MHC I; from RER with help of the B2 microglobulin
12. Name the three opsonins
CRP - C3b - IgM
Type IV
MS - hay fever - SLE - goodpastures
IgG
13. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Lymphocytes
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Its main effect is a defect in Ab opsonization for killing
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
14. What are the function of B cells?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgG
B - T - and NK cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
15. where do somatic hypermutation and class switching occur?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
In the germinal center of secondary follicles (In the paler center)
not Ab mediated
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
16. ________ regulate the cell mediated response.
Kill them because they have CD16 on them that recognize the FcG portion
Fc
Humoral
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
17. What are the autoantibodies for sjorgens syndrome?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti SS- A (anti RO) and Anti SS- B
Anti alpha subunit 3 of collagen on type IV bm
18. Which HLA's are included in MHC I? MHC II?
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19. 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).
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
20. What does IL 10 do? who is secreted by?
Tetanus - Botulinum - HBV - Rabies
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
type four
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
21. What are some catalase positive organisms?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
S. aureus - E. Coli - aspergillus
If there is class switching and plasma cell production (that is when memory cells are produced)
22. What happens in a deficiency of C3?
MHC class molecules bind to KIRS or CD94 to prevent killing
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
23. What are the autoantibodies for systemic sclerosis?
Recom IL 11; thrombocytopenia
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Edema and necrosis in that region
Anti topoisomerase
24. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Rheumatic arthritis
IL 4
25. What is epo used for?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
...
Anemias (esp due to renal failure)
Anti Jo -1
26. What lymph node drains the rectum (above the pectinate line)?
A j chain
Antibody mediated cytotoxicity; either complement dependent or complement independent
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Internal iliac
27. What do mature naive B lymphocytes express?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Lymphocytes
IgM and IgD
Antihistone
28. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Local infection/inflammation; infection of the ln itself; metastasis
neutrophilia!
Antimicrosomal and antithyroglobulin
29. What are the main symptoms of T cell immunodeficiencies?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
IgG
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
30. What is recomb beta interferon used for?
MS
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
Superficial inguinal
31. other than eat and bite RBCs what else do Macrophages of spleen do>
T cell activation; no with CD 4 or CD 8
Remove encapsulated bacateria
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antihistone
32. What lymph node drains the lateral side of the dorsum of the foot?
Cytokine IL 10 secreted by Th2
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
IgG
Popliteal
33. What are the cell surface proteins on NK cells?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Viral neutralization of igM and IgG!
MHC I - CD16 - CD56
A - B - C; all the D's
34. Leukocyte adhesion defect presents with...
Histamine; post capillary venules - vasodilation
Activates cytotoxic CD 8 T cells as second signal
neutrophilia!
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
35. Which type of selection of thymic development provides central tolerance?
TGF beta and IL 10
Negative selection
If there is class switching and plasma cell production (that is when memory cells are produced)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
36. what cell surface marker is used for NK cells as it is unique to them?
Bind FcG for antibody dependent cellular cytotoxicity
CD56
opsonizes
Anti Ach receptor
37. what mediates the type II hypersensitivity? What are the two different methods?
pentamer
Antibody mediated cytotoxicity; either complement dependent or complement independent
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Lymphocytes
38. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
A recomb cytokine of IL 2; RCC and metastatic melanoma
MS - hay fever - SLE - goodpastures
39. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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 and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
40. 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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
MHC I; from RER with help of the B2 microglobulin
Anti glutamate carboxylase and anti insulin
41. Which diseases are associated with DR5?
IgG
Pernicious Anemia and Hashimotos
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
42. What are the autoantibodies for pemphigus bulgaris?
Sinusitis - otitis media - pneumonia
Antidesmoglein
Not thymus - BM
dimer
43. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgA
44. The pathogenesis of contact dermatitis is ________ hypersensitivity
Cross link
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
type four
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
45. Which disease is associated with DR7?
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
Secretory component
Steroid responsive nephrotic syndrome
CD21 on B cells (although there is T cell lymphocytosis in EBV)
46. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
IL 4
Type IV
TNF alpha and IL1
mesenchymal
47. where do NK cells develop?
Not thymus - BM
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Cyclosporine - OKT3
dimer
48. What lymph node drains the sigmoid colon?
Inferior mesenteric
MHC I - CD16 - CD56
Graves
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
49. What are the PALS?
T
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Secretory component
50. What are the two signals to kill for NK cells?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Pernicious Anemia and Hashimotos
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
MHC class molecules bind to KIRS or CD94 to prevent killing
Sorry!:) No result found.
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