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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?
Interferon gamma; Th1
encapsulated
Basophils! THey want IG E class switch!
Fab portion
2. The pathogenesis of contact dermatitis is ________ hypersensitivity
Cyclosporine - OKT3
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
type four
Th2; Th1
3. What is the white pulp of the spleen?
opsonizes
Fab portion
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Sinusitis - otitis media - pneumonia
4. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Previous transfusion; pregnant woman whose fetus had paternal antigens
C5a
Th cells fail to produce interferon gamma; a lot of IgE
5. Which is the most abundant antibody in blood?
DM type I
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IL 4 - 5 - 10 - 6
IgG
6. which of the hypersensitivity reactions is not Ab mediated?
Activates Th1 helper cells; Macrophages
Type IV
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
Receiving preformed Antibodies
7. What lymph node drains the upper limb?
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Cells that stil have weird parts of their membrane that macrophages usually bite off
Axillary
8. What cytokines to Th2 secrete?
Activates Th1 helper cells; Macrophages
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 4 - 5 - 10 - 6
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
9. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Celiac
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgM and IgG
MS - hay fever - SLE - goodpastures
10. Which disease is associated with B8?
2 heavy chains and two light chains
Viral neutralization of igM and IgG!
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
Graves
11. What lymph node drains the thigh?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Superficial inguinal
Local infection/inflammation; infection of the ln itself; metastasis
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
12. what will NK cells do to cells covered in IgG Ab? why?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Kill them because they have CD16 on them that recognize the FcG portion
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Daclizumab; prevent ACUTE rejection of renal transplant
13. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Bind FcG for antibody dependent cellular cytotoxicity
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
Anti alpha subunit 3 of collagen on type IV bm
14. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
No because no peptide fragment!
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
neutrophilia!
15. What is passive immunity?
Alternative splicing of mRNA
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Receiving preformed Antibodies
Yes
16. IgG...
Recom IL 11; thrombocytopenia
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
NK cells
opsonizes
17. which B and T cell disorder presents with specifically low IgM?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Wiskott Aldrich syndrome
18. Which is the main antibody that provides passive immunity to infants?
IgG
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antimicrosomal and antithyroglobulin
CD56
19. 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
Anti TSh receptor
Anti smooth muscle
Previous transfusion; pregnant woman whose fetus had paternal antigens
20. The secondary follicles have __________; primary follicles are dense
IgM and IgA
pale central germinal centers
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Rheumatic arthritis
21. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
No because no peptide fragment!
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)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
22. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Influenza; antigenic shift; antigenic drift
Anti mitochondrial
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
23. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MS
Activates Th1 helper cells; Macrophages
24. Name two endogenous pyrogens
Remove encapsulated bacateria
IL 1 and IL 6
isotype
pale central germinal centers
25. What is the main cytokine that activates eosinophils?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IL 5
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
26. In general What are T cells good for?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti viral and anti tumor
Macrophages - Dendritic cells - B cells
27. Monomer in circulation - ___ when secreted
B - T - and NK cells
dimer
Antimicrosomal and antithyroglobulin
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
28. which antibodies prevent antigens from binding mucosal surfaces?
lowest concentration
Antimicrosomal and antithyroglobulin
B - T - and NK cells
IgA
29. What are MHC's necessary for? By themselves?
MHC class molecules bind to KIRS or CD94 to prevent killing
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
T cell activation; no with CD 4 or CD 8
30. What is colostrum?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Anti IF
The igA found in breast milk
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
31. What is an example of a parasite showing antigenic variation?
Graves
Not thymus - BM
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
32. Which diseases are associated with DR2?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
MS - hay fever - SLE - goodpastures
Negative!
33. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
MHC class molecules bind to KIRS or CD94 to prevent killing
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Graves
34. What is recomb alpha interferon used for?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
type four
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
35. What is the main function of IL 8?
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
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
Recom IL 11; thrombocytopenia
A chemotactic factor for neutrophils
36. The Fc region is found on the...
carboxy terminal
TGF beta and IL 10
Lymphocytes
Superficial inguinal
37. What is immune complex disease? give an example.
Acts as second signal on B cells to induce class switching to IgE and IgG
delayed!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
38. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
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 :(
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Histamine; post capillary venules - vasodilation
TGF beta and IL 10
39. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Rheumatic arthritis
Wiskott Aldrich syndrome
Not thymus - BM
40. What is the toxicity of muromonab?
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
RNA segment reassortment
MS - hay fever - SLE - goodpastures
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
41. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
IL 3; supports growth and differentiation of bone marrow stem cells
IgE; by activating eosinophils
Macrophages - Dendritic cells - B cells
42. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
43. Give an example of someone who could get hyperacute transplant rejection.
NK cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
44. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
delayed!
45. ________ regulate the cell mediated response.
Humoral
T cell precursor
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IL 4 - 5 - 10 - 6
46. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MS - hay fever - SLE - goodpastures
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
Chronic granulomatous disease
Sinusitis - otitis media - pneumonia
47. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
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)
48. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
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
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
T cell dysfunction
49. How is the antigen loaded onto a MHC II?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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
lowest concentration
If there is class switching and plasma cell production (that is when memory cells are produced)
50. What is digoxin immune Fab used for?
NK cells
Antidote for digoxin intoxication
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
By transcytosis
Sorry!:) No result found.
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