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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 happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
False! B cell class switching requires a second signal
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
Paracortex
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
2. Which HLA's are included in MHC I? MHC II?
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3. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Paracortex; viral infection
Not thymus - BM
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
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
4. T/F B cells do not require a second signal
MS - hay fever - SLE - goodpastures
False! B cell class switching requires a second signal
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Rheumatic arthritis
5. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Previous transfusion; pregnant woman whose fetus had paternal antigens
pathogenesis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
6. What is recomb beta interferon used for?
IL 1 and IL 6
Edema and necrosis in that region
MS
Not thymus - BM
7. What lymph node drains the sigmoid colon?
Inferior mesenteric
By transcytosis
Tetanus - Botulinum - HBV - Rabies
Macrophages - Dendritic cells - B cells
8. How fast does it occur?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
A j chain
The patient could become cyanotic in the OR!
type four
9. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
...
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Para aortic
10. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
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
Celiac
11. What happens in a deficiency of C3?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Superficial inguinal
MHC class molecules bind to KIRS or CD94 to prevent killing
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
12. What are the autoantibodies for primary biliary cirrhosis?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti mitochondrial
Negative nitroblue tetrazolium reduction test
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
13. What are the autoantibodies for hashimotos?
Cytokine IL 10 secreted by Th2
Antimicrosomal and antithyroglobulin
Tetanus - Botulinum - HBV - Rabies
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
14. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
...
IgA
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
15. What is the pathology in hyperacute transplant rejection?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Local infection/inflammation; infection of the ln itself; metastasis
16. when can graft versus host disease? What is the result?
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
IL 1 and IL 6
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Kill them because they have CD16 on them that recognize the FcG portion
17. The idiotype; the Fc portion determines the...
isotype
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
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
...
18. in which immunodef order do you see a lot of pus? no pus?
Anti SS- A (anti RO) and Anti SS- B
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
19. What is a factor that is a predictor for a bad transplantation?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
20. which antibody is involved in the primary response or immediate response to an antigen?
IgM
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Popliteal
21. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Macrophages - Dendritic cells - B cells
Alternative splicing of mRNA
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
TNF alpha and IL1
22. Leukocyte adhesion defect presents with...
neutrophilia!
Antidote for digoxin intoxication
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IL 4 - 5 - 10 - 6
23. What is the general structure of an Ab?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
2 heavy chains and two light chains
24. describe the pathogenesis of delayed type IV hypersensitivity
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
Tetanus - Botulinum - HBV - Rabies
Anti TSh receptor
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
25. To what disease do the autoantibodies to IgG (rheumatoid factor)?
The igA found in breast milk
...
IL 1 and IL 6
Rheumatic arthritis
26. Which diseases are associated with DR4?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
DM type I and RA
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
27. What are the symptoms of serum sickness?
A chemotactic factor for neutrophils
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
28. A lymph node is a ________ lymphoid organ.
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
secondary
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
29. What are the PALS?
Cross link
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
Superficial inguinal
30. 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
False! B cell class switching requires a second signal
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
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
31. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Anti Jo -1
Paracortex; viral infection
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
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
32. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
Previous transfusion; pregnant woman whose fetus had paternal antigens
Antimicrosomal and antithyroglobulin
DM type I
33. What are the main cell surface proteins on B cells?
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
Severe pyogenic infections early in life
Negative selection
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
34. How is the thymus organized? what happens in each section?
Basophils! THey want IG E class switch!
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
When you select for which MHC it will have; take out the lymphs that self react
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
35. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Anti smooth muscle
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anti Jo -1
Th cells fail to produce interferon gamma; a lot of IgE
36. What are the autoantibodies for goodpastures syndrome?
Popliteal
S. aureus - E. Coli - aspergillus
Anti alpha subunit 3 of collagen on type IV bm
A - B - C; all the D's
37. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
encapsulated
not Ab mediated
TNF alpha and IL1
38. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Stimulate the liver to release acute phase reactants
Its a serine protease that activates apoptosis; NK and CD8
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
39. The MALT/GALT are not...
encapsulated
TNF alpha and IL1
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Its a serine protease that activates apoptosis; NK and CD8
40. what ensure that a memory response is generated?
Axillary
T cell dysfunction
If there is class switching and plasma cell production (that is when memory cells are produced)
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
41. What is the common variable immunodeficiency ? How is it different from Brutons?
type four
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
Local infection/inflammation; infection of the ln itself; metastasis
42. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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 :(
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
NK cells
43. What is the receptor for EBV? On what cells is that located?
Axillary
IgA
CD21 on B cells (although there is T cell lymphocytosis in EBV)
encapsulated
44. What is the most common selective Ig deficiency? What is the presentation?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
heavy chains
45. The lymphocytes are ________ origin
cannot cross placenta
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
MS
mesenchymal
46. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
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
47. 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
Its main effect is a defect in Ab opsonization for killing
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
carboxy terminal
48. What is the autoantibody for SLE that is nonspecific? Specific?
No because no peptide fragment!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
49. 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
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
IgE; by activating eosinophils
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
50. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
Interferon gamma; Th1
IgM
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