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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.
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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 does IgA pick up from epithelial cells before being secreted?
Activates Th1 helper cells; Macrophages
Secretory component
Celiac
isotype
2. IgG...
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
opsonizes
Antibody mediated cytotoxicity; either complement dependent or complement independent
encapsulated
3. What type of side chains are found on Fc region of an antibody?
If there is class switching and plasma cell production (that is when memory cells are produced)
Carbohydrate
Anti alpha subunit 3 of collagen on type IV bm
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
4. What is the most common example of passive immunity?
delayed!
Anti viral and anti tumor
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IgAs in mothers breast milk!
5. How fast does it occur?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Antihistone
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
The patient could become cyanotic in the OR!
6. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
TGF beta and IL 10
dimer
Its main effect is a defect in Ab opsonization for killing
7. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
8. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
MHC II - B7
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Increases expression of MHC I and MHC II and also activates NK cells
9. What portion of the lymph node is not well developed in DiGeorge Syndrome?
IL 5
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Paracortex
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
10. Other than stimulating fever - what else does IL 6 do?
T cell activation; no with CD 4 or CD 8
Yes
Stimulate the liver to release acute phase reactants
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
11. 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?
Chronic granulomatous disease
CD56
Lymphocytes
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
12. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
Antidesmoglein
No because no peptide fragment!
Bind FcG for antibody dependent cellular cytotoxicity
13. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti IF
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
14. What cytokines are released by Th1 cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IL 4 - 5 - 10 - 6
Interferon gamma and IL 2
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
15. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Paracortex
16. What does interferon gamma do? What two type of cells does it attack mostly?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
MHC I - CD16 - CD56
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
17. What is recomb alpha interferon used for?
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
18. what will NK cells do to cells covered in IgG Ab? why?
Viral neutralization of igM and IgG!
Kill them because they have CD16 on them that recognize the FcG portion
Antimicrosomal and antithyroglobulin
lowest concentration
19. What can cause a lymph node enlargement?
Graves
Local infection/inflammation; infection of the ln itself; metastasis
Recom IL 11; thrombocytopenia
Paracortex
20. How does the alternative pathway lead to MAC activation?
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
By transcytosis
encapsulated
Anti Jo -1
21. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
MS - hay fever - SLE - goodpastures
Activate macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
22. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
S. aureus - E. Coli - aspergillus
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Steroid responsive nephrotic syndrome
23. What are the autoantibodies for drug induced lupus?
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
Increases expression of MHC I and MHC II and also activates NK cells
Antihistone
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
24. What happens in a secondary follicle?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
B - T - and NK cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Glycoproteins; HLA
25. which type of immunity is slow but long lasting? as opposed to...
Previous transfusion; pregnant woman whose fetus had paternal antigens
Active; passive - fast but short half life (3 weeks!)
Paracortex; viral infection
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
26. Which disease is associated with DR7?
MS
Steroid responsive nephrotic syndrome
except hyperacute
Paracortex
27. What is passive immunity?
Antidote for digoxin intoxication
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Receiving preformed Antibodies
MHC I; from RER with help of the B2 microglobulin
28. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Axillary
TNF alpha and IL1
Steroid responsive nephrotic syndrome
Cytokine IL 10 secreted by Th2
29. What are the symptoms of serum sickness?
Hereditary angioedema; PNH
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
pale central germinal centers
30. What are C1 - C2 - C3 - C4 important for?
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
Fab portion
Sinusitis - otitis media - pneumonia
Viral neutralization of igM and IgG!
31. A lymph node is a ________ lymphoid organ.
Active; passive - fast but short half life (3 weeks!)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
secondary
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
32. What are four results of a splenectomy?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Secretory component
Barrel hoop basement membrane fenestrations
33. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
IgM and IgA
Histamine; post capillary venules - vasodilation
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
34. what cell surface marker is used for NK cells as it is unique to them?
IgM and IgA
Increases expression of MHC I and MHC II and also activates NK cells
CD56
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
35. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Acts as second signal on B cells to induce class switching to IgE and IgG
36. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Axillary
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
No because no peptide fragment!
37. The lymphocytes are ________ origin
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
mesenchymal
Anti Ach receptor
IgG
38. 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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Sinusitis - otitis media - pneumonia
Celiac
39. which antibodies prevent antigens from binding mucosal surfaces?
Liver! (they are proteins circulating in the blood)
isotype
Its a serine protease that activates apoptosis; NK and CD8
IgA
40. What is the mechanism for sirolimus? what else it known as?
Alternative splicing of mRNA
heavy chains
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
Its main effect is a defect in Ab opsonization for killing
41. what happens in a deficiency of C1 esterase inhibitor? DAF?
Alternative splicing of mRNA
Hereditary angioedema; PNH
DM type I
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 :(
42. 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!
Its main effect is a defect in Ab opsonization for killing
Celiac
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. What is the main cytokine that activates eosinophils?
S. aureus - E. Coli - aspergillus
neutrophilia!
IL 5
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
44. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti mitochondrial
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Recom IL 11; thrombocytopenia
45. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Delayed type hypersensitivity
46. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
If there is class switching and plasma cell production (that is when memory cells are produced)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Anti glutamate carboxylase and anti insulin
47. What is the pathology of acute transplant rejection? is it reversible?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Lymphocytes
48. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
type four
Basophils! THey want IG E class switch!
SP infections
49. can igG cross the placenta?
Yes
Hemochromatosis
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
pentamer
50. Describe the Mannose Lectin pathway
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Barrel hoop basement membrane fenestrations
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Sorry!:) No result found.
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