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Test your basic knowledge |
USMLE Step 1 Immunology
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Subjects
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health-sciences
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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 are the labs in brutons agammaglobulinemia?
Active; passive - fast but short half life (3 weeks!)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
cannot cross placenta
2. What is the presentation of scid? treatment?
B - T - and NK cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IL 15; IL 12 - interferon Beta and interferon alpha
3. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Yes
Anti glutamate carboxylase and anti insulin
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
4. What does IL 10 do? who is secreted by?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
type four
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 15; IL 12 - interferon Beta and interferon alpha
5. What are the main cell surface proteins on B cells?
dimer
Stimulate the liver to release acute phase reactants
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Negative selection
6. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
False! B cell class switching requires a second signal
encapsulated
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
7. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
neutrophilia!
8. Describe the Mannose Lectin pathway
A chemotactic factor for neutrophils
CD21 on B cells (although there is T cell lymphocytosis in EBV)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
9. What does granzyme do? who secretes it?
pathogenesis
Th2; Th1
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Its a serine protease that activates apoptosis; NK and CD8
10. is IgM an opsonizer?
Remove encapsulated bacateria
Negative!
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
B - T - and NK cells
11. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
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
pathogenesis
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)
12. hat is the presentation of Jobs syndrome or Hyper IgE?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Activate macrophages
13. What is the main function of interferons?
No because no peptide fragment!
Local infection/inflammation; infection of the ln itself; metastasis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
14. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
15. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
cannot cross placenta
type four
T cell dysfunction
16. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Humoral
17. What are the T cell functions?
IgM and IgG
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
Anti SS- A (anti RO) and Anti SS- B
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
18. What is the mechanism for sirolimus? what else it known as?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
opsonizes
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
19. What type of side chains are found on Fc region of an antibody?
CRP - C3b - IgM
Severe pyogenic infections early in life
Complement activation (active in both)
Carbohydrate
20. What is recomb alpha interferon used for?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Barrel hoop basement membrane fenestrations
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti glutamate carboxylase and anti insulin
21. Which HLA's are included in MHC I? MHC II?
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22. which cells have more complete tolerance - B or T cells?
Lymphocytes
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
T
23. What is the pathology seen in chronic transplant rejection?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti mitochondrial
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MS
24. What are the three types of lymphocytes?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
mesenchymal
The patient could become cyanotic in the OR!
B - T - and NK cells
25. What are the two signals required for B cell class switching? Which is the second signal?
Popliteal
Anti viral and anti tumor
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
26. What are the autoantibodies for polymyositis and dermatomyositis?
Superficial inguinal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti Jo -1
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
27. What are the autoantibodies for graves?
Anti TSh receptor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Popliteal
IgM
28. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
not Ab mediated
Macrophages - Dendritic cells - B cells
pentamer
29. The idiotype; the Fc portion determines the...
Anti IF
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
isotype
30. How does the alternative pathway lead to MAC activation?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Secretory component
Axillary
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
31. 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
IL 1 and IL 6
Antibody mediated cytotoxicity; either complement dependent or complement independent
CD21 on B cells (although there is T cell lymphocytosis in EBV)
32. What is Aldesleukin? What is it used for
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
A recomb cytokine of IL 2; RCC and metastatic melanoma
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
33. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
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
IgG
S. aureus - E. Coli - aspergillus
34. 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)?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Negative nitroblue tetrazolium reduction test
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
Recom IL 11; thrombocytopenia
35. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Delayed type hypersensitivity
36. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
dimer
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Popliteal
37. where are complements produced?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
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
Liver! (they are proteins circulating in the blood)
38. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Carbohydrate
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
39. What happens in a secondary follicle?
The igA found in breast milk
Antimicrosomal and antithyroglobulin
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
40. IgG...
Cytokine IL 10 secreted by Th2
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
opsonizes
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
41. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
The patient could become cyanotic in the OR!
C5a
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
42. which interleukin receptor is required for NK development? activation?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IL 15; IL 12 - interferon Beta and interferon alpha
Secretory component
Alternative splicing of mRNA
43. What are the autoantibodies for sjorgens syndrome?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti SS- A (anti RO) and Anti SS- B
44. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Rheumatic arthritis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Immunoflourescent staining of tissue biopsies
45. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
46. What is the most common selective Ig deficiency? What is the presentation?
Secretory component
IgM and IgA
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
47. Leukocyte adhesion defect presents with...
secondary
neutrophilia!
Cyclosporine - OKT3
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!
48. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
MHC I; from RER with help of the B2 microglobulin
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Activates cytotoxic CD 8 T cells as second signal
49. What is the clinical use of Muromonab?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
type four
2 heavy chains and two light chains
Immunosuppression after kidney transplantation
50. Which diseases are associated with DR5?
IgE; by activating eosinophils
Pernicious Anemia and Hashimotos
A j chain
Viral neutralization of igM and IgG!