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Test your basic knowledge |
USMLE Step 1 Immunology
Start Test
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 is thrombopoietin used for?
If there is class switching and plasma cell production (that is when memory cells are produced)
Immunoflourescent staining of tissue biopsies
Thrombocytopenia
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
2. The ______ in the BM are DN - the DP are in the cortex of thymus
Receiving preformed Antibodies
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
T cell precursor
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
3. What is chronic mucocutaneous candidiasis d/t?
lowest concentration
T cell dysfunction
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
4. What are some catalase positive organisms?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
S. aureus - E. Coli - aspergillus
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
lowest concentration
5. What is the toxicity of azathioprine?
...
Bind FcG for antibody dependent cellular cytotoxicity
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
active complement pathway
6. What is the mechanism for sirolimus? what else it known as?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MHC class molecules bind to KIRS or CD94 to prevent killing
lowest concentration
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
7. How do you test for type III hypersensitivity?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Edema and necrosis in that region
Immunoflourescent staining of tissue biopsies
8. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Chronic granulomatous disease
Anti glutamate carboxylase and anti insulin
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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. The Fc region is found on the...
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
...
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
carboxy terminal
10. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antimicrosomal and antithyroglobulin
Inferior mesenteric
11. Leukocyte adhesion defect presents with...
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Barrel hoop basement membrane fenestrations
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
neutrophilia!
12. What lymph node drains the rectum (above the pectinate line)?
MHC class molecules bind to KIRS or CD94 to prevent killing
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Internal iliac
encapsulated
13. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti viral and anti tumor
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Humoral
14. 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)
Anemias (esp due to renal failure)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
T
15. __________ are a part of the innate system.
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
NK cells
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
16. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Sinusitis - otitis media - pneumonia
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgM and IgA
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
17. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
In the germinal center of secondary follicles (In the paler center)
18. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
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
IgG
Anti SS- A (anti RO) and Anti SS- B
19. What is immune complex disease? give an example.
A j chain
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
IgM and IgD
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
20. What are the main Cell surface proteins on T cells?
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
Immunoflourescent staining of tissue biopsies
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
21. What is the clinical use of Muromonab?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Immunosuppression after kidney transplantation
MHC I - CD16 - CD56
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
22. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
23. Name two endogenous pyrogens
pathogenesis
Interferon gamma and IL 2
IL 1 and IL 6
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
24. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
IgAs in mothers breast milk!
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
25. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
Anemias (esp due to renal failure)
Sinusitis - otitis media - pneumonia
26. What is three common causes of severe combined immunodef? What is the result of all three?
TGF beta and IL 10
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Popliteal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
27. what cell surface marker is used for NK cells as it is unique to them?
Glycoproteins; HLA
Anti Jo -1
CD56
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
28. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti mitochondrial
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
29. In thymic development - What is the positive selection? negative selections?
Activates cytotoxic CD 8 T cells as second signal
When you select for which MHC it will have; take out the lymphs that self react
heavy chains
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
30. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti smooth muscle
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
except hyperacute
31. What does IL 10 do? who is secreted by?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cyclosporine - OKT3
Humoral
32. what bacteria are a splenectomy patient most susceptible to? why?
cannot cross placenta
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
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
33. So antibodies are the effectors for the humoral response. List some of their functions.
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Kill them because they have CD16 on them that recognize the FcG portion
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Activate macrophages
34. What is the receptor for EBV? On what cells is that located?
A j chain
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
35. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
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
opsonizes
MHC I; from RER with help of the B2 microglobulin
36. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
isotype
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Complement activation (active in both)
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
37. 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
IgG
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IgA
38. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
T
Its main effect is a defect in Ab opsonization for killing
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
39. What does interferon gamma do to be antiviral?
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
Immunosuppression after kidney transplantation
NK cells
Increases expression of MHC I and MHC II and also activates NK cells
40. What are the autoantibodies for pernicious anemia?
IL 1 and IL 6
Anti IF
No because no peptide fragment!
In the germinal center of secondary follicles (In the paler center)
41. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
secondary
heavy chains
42. What does interferon gamma do? What two type of cells does it attack mostly?
IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
DM type I and RA
lowest concentration
43. Which type of selection of thymic development provides central tolerance?
Negative selection
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Daclizumab; prevent ACUTE rejection of renal transplant
IgG
44. The pathogenesis of contact dermatitis is ________ hypersensitivity
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anti Jo -1
type four
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
45. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
IgM and IgD
IL 4
Acts as second signal on B cells to induce class switching to IgE and IgG
46. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Lymphocytes
TLR ad nuclear receptors
Daclizumab; prevent ACUTE rejection of renal transplant
47. Give an example of someone who could get hyperacute transplant rejection.
No because no peptide fragment!
Steroid responsive nephrotic syndrome
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Previous transfusion; pregnant woman whose fetus had paternal antigens
48. What is the pathogenesis of a hypersensitivity reaction?
MHC I - CD16 - CD56
A recomb cytokine of IL 2; RCC and metastatic melanoma
MHC class molecules bind to KIRS or CD94 to prevent killing
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
49. What are the cell surface proteins on NK cells?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
MHC I - CD16 - CD56
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
50. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Influenza; antigenic shift; antigenic drift
Axillary