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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
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 is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
T cell precursor
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
Pernicious Anemia and Hashimotos
2. What are target cells?
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
Macrophages - Dendritic cells - B cells
type four
Cells that stil have weird parts of their membrane that macrophages usually bite off
3. The two heavy chains of an antibody contribute to the...
Fab portion
IL 4
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
4. can igG cross the placenta?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
Yes
5. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Activates Th1 helper cells; Macrophages
6. What is the presentation of Brutons agammaglobulinemia?
Humoral
Active; passive - fast but short half life (3 weeks!)
Severe pyogenic infections early in life
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
7. Which HLA's are included in MHC I? MHC II?
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8. What is thrombopoietin used for?
If there is class switching and plasma cell production (that is when memory cells are produced)
Thrombocytopenia
Viral neutralization of igM and IgG!
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
9. What is an example of a parasite showing antigenic variation?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Celiac
10. What does granulysin do?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
SP infections
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
11. What lymph node drains the scrotum?
DM type I
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Superficial inguinal
12. What are the main symptoms of T cell immunodeficiencies?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgM and IgD
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
13. Which antibodies can be multimeric?
IgM and IgA
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Glycoproteins; HLA
14. What is chronic mucocutaneous candidiasis d/t?
IgE
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
T cell dysfunction
15. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Interferon gamma; Th1
Paracortex; viral infection
16. 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
The igA found in breast milk
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Carbohydrate
17. What is epo used for?
Hemochromatosis
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
Anemias (esp due to renal failure)
The igA found in breast milk
18. In general What are T cells good for?
Anti viral and anti tumor
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
19. How does complement link innate and adaptive?
IL 3; supports growth and differentiation of bone marrow stem cells
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
When you select for which MHC it will have; take out the lymphs that self react
S. aureus - E. Coli - aspergillus
20. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
IgM and IgD
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Interferon gamma and IL 2
21. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Paracortex; viral infection
Anti topoisomerase
IgG
22. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
Superficial inguinal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
23. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Remove encapsulated bacateria
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
24. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Paracortex
25. What happens in a secondary follicle?
encapsulated
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Th2; Th1
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
26. What does IL 10 do? who is secreted by?
Severe pyogenic infections early in life
Histamine; post capillary venules - vasodilation
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Anti TSh receptor
27. What is the marginal zone of the spleen? what happens there?
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
...
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
IgG
28. What are the autoantibodies for systemic sclerosis?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti topoisomerase
pale central germinal centers
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
29. what secretes IL 4?
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
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Basophils! THey want IG E class switch!
30. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
No because no peptide fragment!
IgG
Sinusitis - otitis media - pneumonia
31. Which cytokines do Th2 release and For what?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IL 4
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
32. What is hereditary angioedema? What are the C3 levels?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Cyclosporine - OKT3
33. How is i Th1 helper cell inhibited?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Cytokine IL 10 secreted by Th2
Glycoproteins; HLA
34. what bacteria are a splenectomy patient most susceptible to? why?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Steroid responsive nephrotic syndrome
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
Superficial inguinal
35. Name two endogenous pyrogens
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IL 1 and IL 6
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
C5a
36. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
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
Anti mitochondrial
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
37. From where do cytokines come from?
A - B - C; all the D's
Superior mesenteric
Superficial inguinal
Lymphocytes
38. which cytokine inhibits TH2 cells? secreted by who?
...
IgAs in mothers breast milk!
Interferon gamma; Th1
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
39. when can graft versus host disease? What is the result?
Anti mitochondrial
Influenza; antigenic shift; antigenic drift
Tetanus - Botulinum - HBV - Rabies
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
40. ________ regulate the cell mediated response.
Cells that stil have weird parts of their membrane that macrophages usually bite off
Humoral
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
41. So antibodies are the effectors for the humoral response. List some of their functions.
MS - hay fever - SLE - goodpastures
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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
42. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
A - B - C; all the D's
pathogenesis
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
43. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
Rheumatic arthritis
All MHC 1/CD8
MS
44. What is Aldesleukin? What is it used for
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Paracortex
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
A recomb cytokine of IL 2; RCC and metastatic melanoma
45. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Hemochromatosis
A chemotactic factor for neutrophils
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
46. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
NK cells
delayed!
47. Which type of selection of thymic development provides central tolerance?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Negative selection
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
48. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Immunosuppression after kidney transplantation
Tetanus - Botulinum - HBV - Rabies
49. To what portion of the Antibody do the complements bind?
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)
Humoral
Receiving preformed Antibodies
Fc
50. What lymph node drains the anal canal (below the pectinate line)?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Superficial inguinal
Type IV
Kill them because they have CD16 on them that recognize the FcG portion