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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 secretes IL 4?
CD56
Anti Jo -1
Basophils! THey want IG E class switch!
Chronic granulomatous disease
2. What are the autoantibodies for hashimotos?
IL 5
DM type I and RA
Antimicrosomal and antithyroglobulin
carboxy terminal
3. what ensure that a memory response is generated?
Antihistone
If there is class switching and plasma cell production (that is when memory cells are produced)
IgE; by activating eosinophils
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
4. What are the two signals required for Th1 cells? what happens after then activated?
MHC I; from RER with help of the B2 microglobulin
Macrophages - Dendritic cells - B cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti topoisomerase
5. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Local infection/inflammation; infection of the ln itself; metastasis
C5a
MS
6. What do mature naive B lymphocytes express?
SP infections
pale central germinal centers
IgM and IgD
B - T - and NK cells
7. What are the three types of APCs?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Macrophages - Dendritic cells - B cells
dimer
active complement pathway
8. Which helper T cells' development is induced by IL 4? IL 12?
Paracortex
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Th2; Th1
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
9. What is epo used for?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Hemochromatosis
Anemias (esp due to renal failure)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
10. The alternative pathway is the only constutively...
Activates Th1 helper cells; Macrophages
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
active complement pathway
delayed!
11. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Thrombocytopenia
2 heavy chains and two light chains
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
12. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
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
IgG
isotype
13. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
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
Negative!
Celiac
14. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
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
Celiac
15. The MALT/GALT are not...
Antidesmoglein
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
encapsulated
Steroid responsive nephrotic syndrome
16. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
IgE; by activating eosinophils
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
17. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Anti TSh receptor
A - B - C; all the D's
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti alpha subunit 3 of collagen on type IV bm
18. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Hemochromatosis
Negative!
Activates Th1 helper cells; Macrophages
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
19. What is the main cytokine that activates eosinophils?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IL 5
Axillary
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
20. What are the two signals required for B cell class switching? Which is the second signal?
Rheumatic arthritis
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Edema and necrosis in that region
21. What are the autoantibodies for primary biliary cirrhosis?
MS - hay fever - SLE - goodpastures
Fab portion
Anti mitochondrial
Paracortex
22. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
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
Severe pyogenic infections early in life
23. IgM can exist as a _______ also
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Fab portion
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
pentamer
24. what will NK cells do to cells covered in IgG Ab? why?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IL 1 and IL 6
Kill them because they have CD16 on them that recognize the FcG portion
25. What does granzyme do? who secretes it?
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Its a serine protease that activates apoptosis; NK and CD8
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
26. What is recomb alpha interferon used for?
C5a
lowest concentration
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
27. which antibodies can bind complement?
T
Complement activation (active in both)
By transcytosis
IgM and IgG
28. What are the main Cell surface proteins on T cells?
Superficial inguinal
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
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
29. What is passive immunity?
Anti mitochondrial
Receiving preformed Antibodies
Antihistone
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
30. Only the _______ contribute to the Fc region
Recom IL 11; thrombocytopenia
Activate macrophages
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
heavy chains
31. What lymph node drains the scrotum?
Rheumatic arthritis
IL 1 and IL 6
By transcytosis
Superficial inguinal
32. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Anti Ach receptor
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
Activate macrophages
NK cells
33. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
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
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
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
34. which of the transplant rejections is antibody mediated? why does it occur?
neutrophilia!
Anti Jo -1
The igA found in breast milk
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
35. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
Anti topoisomerase
NK cells
Viral neutralization of igM and IgG!
36. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
IL 15; IL 12 - interferon Beta and interferon alpha
Type IV
Barrel hoop basement membrane fenestrations
37. Which MHC presents intracellular peptides? how so?
CD56
RNA segment reassortment
MHC I; from RER with help of the B2 microglobulin
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
38. How is the antigen loaded onto a MHC II?
Anti mitochondrial
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
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
39. IgG...
Immunoflourescent staining of tissue biopsies
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti topoisomerase
opsonizes
40. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
MHC I - CD16 - CD56
In the germinal center of secondary follicles (In the paler center)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
41. What lymph node drains the lateral side of the dorsum of the foot?
Paracortex; viral infection
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Popliteal
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
42. which cells have more complete tolerance - B or T cells?
Antibody mediated cytotoxicity; either complement dependent or complement independent
MHC class molecules bind to KIRS or CD94 to prevent killing
Remove encapsulated bacateria
T
43. __________ are a part of the innate system.
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
Anti U1 RNP (ribonucleoprotein)
NK cells
Lymphocytes
44. Other than stimulating fever - what else does IL 6 do?
MHC I - CD16 - CD56
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
isotype
Stimulate the liver to release acute phase reactants
45. What are the function of B cells?
Antidote for digoxin intoxication
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
46. What is hereditary angioedema? What are the C3 levels?
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
Internal iliac
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
47. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Axillary
48. what bacteria are a splenectomy patient most susceptible to? why?
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Secretory component
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
49. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Thrombocytopenia
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
50. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
In the germinal center of secondary follicles (In the paler center)
IgM
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
The igA found in breast milk
Sorry!:) No result found.
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