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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
Subjects
:
health-sciences
,
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. 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
Acts as second signal on B cells to induce class switching to IgE and IgG
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Superior mesenteric
2. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Lymphocytes
Paracortex
dimer
3. which B and T cell disorder presents with specifically low IgM?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Wiskott Aldrich syndrome
Anti smooth muscle
Chronic granulomatous disease
4. What is the pathogenesis of acute transplant rejection? When does it occur?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
A recomb cytokine of IL 2; RCC and metastatic melanoma
opsonizes
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
5. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
Activate macrophages
TLR ad nuclear receptors
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
6. What do multimeric antibodies require for assembly?
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
A j chain
Basophils! THey want IG E class switch!
Axillary
7. What lymph node drains the anal canal (below the pectinate line)?
Receiving preformed Antibodies
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Superficial inguinal
IgE
8. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Remove encapsulated bacateria
IL 1 and IL 6
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
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
9. what cell surface marker is used for NK cells as it is unique to them?
CD56
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Acts as second signal on B cells to induce class switching to IgE and IgG
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
10. What is the main function of TNF alpha? How does it do this?
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
12. Name two endogenous pyrogens
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti glutamate carboxylase and anti insulin
Anti TSh receptor
IL 1 and IL 6
13. What is an example of a parasite showing antigenic variation?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Increases expression of MHC I and MHC II and also activates NK cells
Anti TSh receptor
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
14. What are the three types of lymphocytes?
B - T - and NK cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
pathogenesis
Remove encapsulated bacateria
15. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Increases expression of MHC I and MHC II and also activates NK cells
All MHC 1/CD8
16. Leukocyte adhesion defect presents with...
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
neutrophilia!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
17. Monomer in circulation - ___ when secreted
Lymphocytes
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
dimer
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
18. What lymph node drains the stomach?
Anti Ach receptor
Celiac
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
19. Which HLA's are included in MHC I? MHC II?
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20. What is recomb beta interferon used for?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MS
lowest concentration
21. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Activates Th1 helper cells; Macrophages
Wiskott Aldrich syndrome
Paracortex; viral infection
22. What is the clinical use for azathioprine?
Internal iliac
...
Cross link
dimer
23. What are the PALS?
dimer
MHC II - B7
Recom IL 11; thrombocytopenia
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
24. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
25. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Glycoproteins; HLA
Th cells fail to produce interferon gamma; a lot of IgE
B - T - and NK cells
TGF beta and IL 10
26. what characterizes an arthus reaction?
When you select for which MHC it will have; take out the lymphs that self react
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
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
Edema and necrosis in that region
27. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
DM type I and RA
28. What is the autoantibody for SLE that is nonspecific? Specific?
Anti Ach receptor
Para aortic
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
29. What is colostrum?
Wiskott Aldrich syndrome
The igA found in breast milk
False! B cell class switching requires a second signal
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
30. What is the toxicity of muromonab?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Lymphocytes
A - B - C; all the D's
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
31. other than C3a - what other complement acts as an anaphyloxin?
Anti U1 RNP (ribonucleoprotein)
Remove encapsulated bacateria
C5a
NK cells
32. What are the autoantibodies for myasthenia gravis?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Anti Ach receptor
All MHC 1/CD8
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
33. what bacteria are a splenectomy patient most susceptible to? why?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgM and IgA
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
Thrombocytopenia
34. What lymph node drains the upper limb?
Type IV
Active; passive - fast but short half life (3 weeks!)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Axillary
35. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
neutrophilia!
Alternative splicing of mRNA
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
Rheumatic arthritis
36. What are target cells?
Daclizumab; prevent ACUTE rejection of renal transplant
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cells that stil have weird parts of their membrane that macrophages usually bite off
type four
37. What are the main Cell surface proteins on T cells?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MS
38. What is the general structure of an Ab?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
2 heavy chains and two light chains
Para aortic
39. What is the pathology of acute transplant rejection? is it reversible?
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
Anti glutamate carboxylase and anti insulin
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Its a serine protease that activates apoptosis; NK and CD8
40. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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 :(
T cell activation; no with CD 4 or CD 8
The patient could become cyanotic in the OR!
41. What type of side chains are found on Fc region of an antibody?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Carbohydrate
Basophils! THey want IG E class switch!
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
42. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antihistone
IL 4 - 5 - 10 - 6
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
43. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Increases expression of MHC I and MHC II and also activates NK cells
Rheumatic arthritis
Cross link
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
44. What is the defect in hyper IgM syndrome? What are the lab results?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
IgM and IgD
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
45. What is the main cytokine released by T cells? What does it do
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
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
IL 3; supports growth and differentiation of bone marrow stem cells
46. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Superior mesenteric
Anti Ach receptor
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
47. What are the autoantibodies for drug induced lupus?
encapsulated
Antihistone
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 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
48. In thymic development - What is the positive selection? negative selections?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
When you select for which MHC it will have; take out the lymphs that self react
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Activates Th1 helper cells; Macrophages
49. where do somatic hypermutation and class switching occur?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Glycoproteins; HLA
Humoral
In the germinal center of secondary follicles (In the paler center)
50. Which MHC presents intracellular peptides? how so?
CRP - C3b - IgM
Cytokine IL 10 secreted by Th2
MHC I; from RER with help of the B2 microglobulin
TGF beta and IL 10