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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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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. which antibody activate mast cells - basophils - and eosinophils?
Paracortex
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IgE
2. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Bind FcG for antibody dependent cellular cytotoxicity
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
3. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
encapsulated
Interferon gamma; Th1
4. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
CRP - C3b - IgM
Cyclosporine - OKT3
5. Which HLA's are included in MHC I? MHC II?
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6. other than mediating shock - what else does TNF alpha do? who releases it mainly?
IgE
Antimicrosomal and antithyroglobulin
Activates Th1 helper cells; Macrophages
Negative selection
7. What are the autoantibodies for Celiac disease?
Kill them because they have CD16 on them that recognize the FcG portion
Bind FcG for antibody dependent cellular cytotoxicity
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
8. What is the cause of thymic aplasia? What is its presentation? What are the labs?
No because no peptide fragment!
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
MHC II - B7
9. __________ are a part of the innate system.
acute phase reactants
NK cells
lowest concentration
Anti Jo -1
10. What type of side chains are found on Fc region of an antibody?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Carbohydrate
A chemotactic factor for neutrophils
Antimicrosomal and antithyroglobulin
11. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
12. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
CRP - C3b - IgM
isotype
Acts as second signal on B cells to induce class switching to IgE and IgG
13. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Negative selection
Interferon gamma and IL 2
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
14. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Severe pyogenic infections early in life
...
15. What are the autoantibodies for myasthenia gravis?
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!
Anti Ach receptor
...
The patient could become cyanotic in the OR!
16. What is epo used for?
Tetanus - Botulinum - HBV - Rabies
Anemias (esp due to renal failure)
Internal iliac
Inferior mesenteric
17. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
MS - hay fever - SLE - goodpastures
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IL 1 and IL 6
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
18. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC I; from RER with help of the B2 microglobulin
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
19. What does IL 10 do? who is secreted by?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Severe pyogenic infections early in life
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
False! B cell class switching requires a second signal
20. What is the pathogenesis of a candida skin test?
Receiving preformed Antibodies
Delayed type hypersensitivity
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
21. What bugs can actually infect the lymph node itself?
The igA found in breast milk
except hyperacute
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
22. What is the presentation of Brutons agammaglobulinemia?
IgAs in mothers breast milk!
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Para aortic
23. How does the alternative pathway lead to MAC activation?
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
Anti glutamate carboxylase and anti insulin
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
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
24. What portion of the lymph node is not well developed in DiGeorge Syndrome?
IgM and IgD
Paracortex
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Basophils! THey want IG E class switch!
25. hat is the presentation of Jobs syndrome or Hyper IgE?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Kill them because they have CD16 on them that recognize the FcG portion
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
26. Which diseases are associated with DR4?
except hyperacute
DM type I and RA
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
dimer
27. Which antibody mediates immunity to worms? how?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Fc
All MHC 1/CD8
IgE; by activating eosinophils
28. in which immunodef order do you see a lot of pus? no pus?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
29. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
30. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
MHC I - CD16 - CD56
T
31. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti mitochondrial
32. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
By transcytosis
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
Antihistone
33. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Popliteal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Bind FcG for antibody dependent cellular cytotoxicity
Alternative splicing of mRNA
34. The ______ in the BM are DN - the DP are in the cortex of thymus
Influenza; antigenic shift; antigenic drift
T cell precursor
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Steroid responsive nephrotic syndrome
35. The pathogenesis of contact dermatitis is ________ hypersensitivity
Stimulate the liver to release acute phase reactants
Type IV
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
type four
36. What lymph node drains the anal canal (below the pectinate line)?
Chronic granulomatous disease
Superficial inguinal
Tetanus - Botulinum - HBV - Rabies
Interferon gamma; Th1
37. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Local infection/inflammation; infection of the ln itself; metastasis
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Alternative splicing of mRNA
38. what ensure that a memory response is generated?
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
False! B cell class switching requires a second signal
If there is class switching and plasma cell production (that is when memory cells are produced)
Basophils! THey want IG E class switch!
39. From where do cytokines come from?
Lymphocytes
Anti glutamate carboxylase and anti insulin
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
40. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Negative!
Anti Ach receptor
41. What are the T cell functions?
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
CRP - C3b - IgM
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Remove encapsulated bacateria
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Influenza; antigenic shift; antigenic drift
...
43. What is the late phase reaction of anaphylaxis allergy? what mediates it?
B - T - and NK cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Negative selection
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)
44. Which cytokines do Th2 release and For what?
Para aortic
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
All MHC 1/CD8
45. Which is the main antibody that provides passive immunity to infants?
Rheumatic arthritis
IgG
Sinusitis - otitis media - pneumonia
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)
46. What lymph node drains the sigmoid colon?
Inferior mesenteric
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Paracortex; viral infection
47. What are the autoantibodies for drug induced lupus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antihistone
except hyperacute
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
48. What are the autoantibodies for goodpastures syndrome?
pale central germinal centers
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
Anti alpha subunit 3 of collagen on type IV bm
49. where are complements produced?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Steroid responsive nephrotic syndrome
Liver! (they are proteins circulating in the blood)
50. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
carboxy terminal
In the germinal center of secondary follicles (In the paler center)
Severe pyogenic infections early in life
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