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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 is the pathology of acute transplant rejection? is it reversible?
Sinusitis - otitis media - pneumonia
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
2. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Paracortex
Edema and necrosis in that region
NK cells
Daclizumab; prevent ACUTE rejection of renal transplant
3. How does the alternative pathway lead to MAC activation?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
Anti topoisomerase
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
4. The MALT/GALT are not...
The igA found in breast milk
encapsulated
Anti smooth muscle
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
5. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgG
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
6. What are the T cell functions?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
opsonizes
7. describe the classic complement pathway.
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
CD56
IL 3; supports growth and differentiation of bone marrow stem cells
8. What can cause a lymph node enlargement?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Superficial inguinal
TLR ad nuclear receptors
Local infection/inflammation; infection of the ln itself; metastasis
9. Which are the only two antiinflammatory cytokines?
SP infections
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
TGF beta and IL 10
10. what cell surface proteins are on all APCs?
Bind FcG for antibody dependent cellular cytotoxicity
IgAs in mothers breast milk!
MHC II - B7
Glycoproteins; HLA
11. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgM
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Paracortex
12. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
Anemias (esp due to renal failure)
Acts as second signal on B cells to induce class switching to IgE and IgG
Not thymus - BM
13. What lymph node drains the stomach?
Celiac
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
Viral neutralization of igM and IgG!
Glycoproteins; HLA
14. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
pathogenesis
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
15. 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?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Tetanus - Botulinum - HBV - Rabies
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
16. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
T cell activation; no with CD 4 or CD 8
Paracortex; viral infection
Yes
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
17. which antibody activate mast cells - basophils - and eosinophils?
Superficial inguinal
IgE
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
18. What is the clinical use for sirolimus? what should you combine it with?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Anti mitochondrial
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
19. can igG cross the placenta?
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Yes
Cells that stil have weird parts of their membrane that macrophages usually bite off
20. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
TNF alpha and IL1
21. What are some sinopulmonary infections?
TGF beta and IL 10
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Sinusitis - otitis media - pneumonia
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
22. in which immunodef order do you see a lot of pus? no pus?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MHC II - B7
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
23. What lymph node drains the testes?
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
TGF beta and IL 10
Para aortic
Anti mitochondrial
24. Which diseases are associated with DR5?
Delayed type hypersensitivity
Pernicious Anemia and Hashimotos
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
25. what cell surface marker is used for NK cells as it is unique to them?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Chronic granulomatous disease
CD56
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
26. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
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
27. T/F B cells do not require a second signal
Fab portion
False! B cell class switching requires a second signal
Negative!
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 :(
28. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Influenza; antigenic shift; antigenic drift
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
29. __________ are a part of the innate system.
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
NK cells
Interferon gamma; Th1
30. What are the autoantibodies for wegeners granulomatosis?
Antibody mediated cytotoxicity; either complement dependent or complement independent
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Humoral
Wiskott Aldrich syndrome
31. What is thrombopoietin used for?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Thrombocytopenia
carboxy terminal
...
32. What is an example of a parasite showing antigenic variation?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cells that stil have weird parts of their membrane that macrophages usually bite off
33. What is the main function of IL 8?
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
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
A chemotactic factor for neutrophils
Its a serine protease that activates apoptosis; NK and CD8
34. What are the main symptoms of B cell immunodeficiencies?
SP infections
Yes
Internal iliac
Acts as second signal on B cells to induce class switching to IgE and IgG
35. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Negative!
If there is class switching and plasma cell production (that is when memory cells are produced)
36. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
IL 1 and IL 6
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
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
37. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Its main effect is a defect in Ab opsonization for killing
Delayed type hypersensitivity
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
38. From where do cytokines come from?
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
secondary
Lymphocytes
39. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Inferior mesenteric
A j chain
40. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
MHC I - CD16 - CD56
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
cannot cross placenta
41. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Complement activation (active in both)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
42. Name the three opsonins
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
CRP - C3b - IgM
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
A - B - C; all the D's
43. Complements are...
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
acute phase reactants
44. What are C1 - C2 - C3 - C4 important for?
NK cells
Yes
Viral neutralization of igM and IgG!
lowest concentration
45. Give an example of someone who could get hyperacute transplant rejection.
Anti U1 RNP (ribonucleoprotein)
Barrel hoop basement membrane fenestrations
Previous transfusion; pregnant woman whose fetus had paternal antigens
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
46. How is the antigen loaded onto a MHC II?
Barrel hoop basement membrane fenestrations
Acts as second signal on B cells to induce class switching to IgE and IgG
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
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
47. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Anti smooth muscle
Cross link
48. Which disease is associated with DR7?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Steroid responsive nephrotic syndrome
49. 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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Rheumatic arthritis
50. what mediates the type II hypersensitivity? What are the two different methods?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Antibody mediated cytotoxicity; either complement dependent or complement independent
Sorry!:) No result found.
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