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Test your basic knowledge |
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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study here
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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 is the late phase reaction of anaphylaxis allergy? what mediates it?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Humoral
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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)
2. What are the two signals required for B cell class switching? Which is the second signal?
Anti IF
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
TLR ad nuclear receptors
3. 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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
opsonizes
Delayed type hypersensitivity
4. What is the pathogenesis of acute transplant rejection? When does it occur?
T cell dysfunction
IgM and IgG
Axillary
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
5. other than eat and bite RBCs what else do Macrophages of spleen do>
Active; passive - fast but short half life (3 weeks!)
Remove encapsulated bacateria
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Activates Th1 helper cells; Macrophages
6. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Tetanus - Botulinum - HBV - Rabies
7. Type Iv hypersensitivity is...
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Type IV
T cell precursor
delayed!
8. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Receiving preformed Antibodies
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
9. other than C3a - what other complement acts as an anaphyloxin?
C5a
Superior mesenteric
Viral neutralization of igM and IgG!
Receiving preformed Antibodies
10. What lymph node drains the lateral side of the dorsum of the foot?
...
Popliteal
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
11. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
lowest concentration
IgM
Interferon gamma and IL 2
12. What is serum sickness? give an example.
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
2 heavy chains and two light chains
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
13. What is the most common example of passive immunity?
MS - hay fever - SLE - goodpastures
Activates Th1 helper cells; Macrophages
IgAs in mothers breast milk!
Wiskott Aldrich syndrome
14. What is the clinical use for sirolimus? what should you combine it with?
except hyperacute
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
All MHC 1/CD8
15. What are the autoantibodies for drug induced lupus?
The igA found in breast milk
Antihistone
DM type I
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
16. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Secretory component
Chronic granulomatous disease
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
17. what will NK cells do to cells covered in IgG Ab? why?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Kill them because they have CD16 on them that recognize the FcG portion
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
18. give an example of how influenza does a major antigenic shift.
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
IgG
RNA segment reassortment
Recom IL 11; thrombocytopenia
19. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
20. To what portion of the Antibody do the complements bind?
Fc
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cyclosporine - OKT3
21. T/F B cells do not require a second signal
Receiving preformed Antibodies
Basophils! THey want IG E class switch!
Fab portion
False! B cell class switching requires a second signal
22. What are the autoantibodies for Celiac disease?
carboxy terminal
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
23. What is the most common selective Ig deficiency? What is the presentation?
Fc
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Cross link
Paracortex; viral infection
24. which B and T cell disorder presents with specifically low IgM?
Superior mesenteric
If there is class switching and plasma cell production (that is when memory cells are produced)
MS - hay fever - SLE - goodpastures
Wiskott Aldrich syndrome
25. 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?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
Carbohydrate
Anti mitochondrial
26. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Axillary
Activate macrophages
Yes
27. which of the hypersensitivity reactions is not Ab mediated?
acute phase reactants
MS - hay fever - SLE - goodpastures
Type IV
SP infections
28. What is digoxin immune Fab used for?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Antidote for digoxin intoxication
Humoral
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
29. what bacteria are a splenectomy patient most susceptible to? why?
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
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
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
30. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
pathogenesis
TNF alpha and IL1
DM type I and RA
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
31. How fast does it occur?
Antidote for digoxin intoxication
The patient could become cyanotic in the OR!
Anti glutamate carboxylase and anti insulin
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
32. The ______ in the BM are DN - the DP are in the cortex of thymus
Rheumatic arthritis
Anti smooth muscle
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
T cell precursor
33. Which antibodies can be multimeric?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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
IgM and IgA
Interferon gamma; Th1
34. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgAs in mothers breast milk!
TNF alpha and IL1
35. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
DM type I and RA
2 heavy chains and two light chains
Cells that stil have weird parts of their membrane that macrophages usually bite off
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
36. what cell surface proteins are on all APCs?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
delayed!
MHC II - B7
37. The MALT/GALT are not...
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Chronic granulomatous disease
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
encapsulated
38. Only the _______ contribute to the Fc region
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
opsonizes
heavy chains
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
39. What lymph node drains the testes?
T cell precursor
Para aortic
Anti U1 RNP (ribonucleoprotein)
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
40. What is the main cytokine that activates eosinophils?
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
NK cells
IL 5
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
41. What lymph node drains the scrotum?
Superficial inguinal
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
B - T - and NK cells
42. How is the thymus organized? what happens in each section?
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
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
Stimulate the liver to release acute phase reactants
MS
43. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
S. aureus - E. Coli - aspergillus
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
IgM and IgD
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
44. What are the mediators that mast cells release?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Receiving preformed Antibodies
45. What is an example of a parasite showing antigenic variation?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti glutamate carboxylase and anti insulin
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti TSh receptor
46. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti U1 RNP (ribonucleoprotein)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MS
47. What are the two signals to kill for NK cells?
A - B - C; all the D's
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Graves
48. Which disease is associated with DR7?
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!
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Complement activation (active in both)
Steroid responsive nephrotic syndrome
49. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
CD56
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 :(
Cross link
Anti smooth muscle
50. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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