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USMLE Step 1 Immunology

Subjects : health-sciences, 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 are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgAs in mothers breast milk!

2. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Local infection/inflammation; infection of the ln itself; metastasis
If there is class switching and plasma cell production (that is when memory cells are produced)
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

3. What is the pathogenesis of acute transplant rejection? When does it occur?
IgM
All MHC 1/CD8
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

4. The lymphocytes are ________ origin
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
Increases expression of MHC I and MHC II and also activates NK cells
mesenchymal

5. Only the _______ contribute to the Fc region
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
Wiskott Aldrich syndrome
heavy chains

6. Describe the Mannose Lectin pathway
Immunosuppression after kidney transplantation
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
B - T - and NK cells

7. What is the toxicity of muromonab?
pale central germinal centers
T cell activation; no with CD 4 or CD 8
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

8. What happens in a secondary follicle?
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

9. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
A - B - C; all the D's
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
RNA segment reassortment

10. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
T
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
delayed!

11. What are the main symptoms of T cell immunodeficiencies?
Activate macrophages
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

12. How is the thymus organized? what happens in each section?
Antidesmoglein
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
IgE

13. What can cause a lymph node enlargement?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Local infection/inflammation; infection of the ln itself; metastasis
DM type I
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

14. what results in symptoms of shock in an acute hemolytic transfusion reaction?
IL 1 and IL 6
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Kill them because they have CD16 on them that recognize the FcG portion
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

15. What are howell jolly bodies?
Anti U1 RNP (ribonucleoprotein)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

16. is IgM an opsonizer?
Negative!
Para aortic
not Ab mediated
Remove encapsulated bacateria

17. What is the defect in hyper IgM syndrome? What are the lab results?
dimer
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CRP - C3b - IgM
Antimicrosomal and antithyroglobulin

18. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Paracortex
Anti alpha subunit 3 of collagen on type IV bm
except hyperacute

19. What does interferon gamma do? What two type of cells does it attack mostly?
neutrophilia!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Increases expression of MHC I and MHC II and also activates NK cells
Bind FcG for antibody dependent cellular cytotoxicity

20. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

21. What is the cause of thymic aplasia? What is its presentation? What are the labs?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
TLR ad nuclear receptors
A j chain

22. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
not Ab mediated
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

23. which cells have more complete tolerance - B or T cells?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T
IgG
Its main effect is a defect in Ab opsonization for killing

24. What kinds of receptors activate innate immunity?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IL 3; supports growth and differentiation of bone marrow stem cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
TLR ad nuclear receptors

25. Give an example of someone who could get hyperacute transplant rejection.
Severe pyogenic infections early in life
Rheumatic arthritis
Previous transfusion; pregnant woman whose fetus had paternal antigens
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 :(

26. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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

27. What type of fenestrations are found in the red pulp of the spleen?
IgAs in mothers breast milk!
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
MHC I; from RER with help of the B2 microglobulin
Barrel hoop basement membrane fenestrations

28. Which helper T cells' development is induced by IL 4? IL 12?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Superficial inguinal
Th2; Th1

29. What lymph node drains the stomach?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Celiac
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
Superficial inguinal

30. What is the presentation of Brutons agammaglobulinemia?
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Bind FcG for antibody dependent cellular cytotoxicity

31. __________ are a part of the innate system.
Hemochromatosis
NK cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IgA

32. What is chronic mucocutaneous candidiasis d/t?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Superficial inguinal
T cell dysfunction
If there is class switching and plasma cell production (that is when memory cells are produced)

33. Type Iv hypersensitivity is...
IgM and IgA
delayed!
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Cytokine IL 10 secreted by Th2

34. what bacteria are a splenectomy patient most susceptible to? why?
Secretory component
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
T cell activation; no with CD 4 or CD 8
Steroid responsive nephrotic syndrome

35. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Activates cytotoxic CD 8 T cells as second signal
Popliteal
Stimulate the liver to release acute phase reactants
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

36. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Rheumatic arthritis
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
Lymphocytes

37. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
lowest concentration
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

38. How does the alternative pathway lead to MAC activation?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Cells that stil have weird parts of their membrane that macrophages usually bite off
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

39. How do you test for type III hypersensitivity?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Immunoflourescent staining of tissue biopsies
A - B - C; all the D's
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

40. which antibody activate mast cells - basophils - and eosinophils?
IgE
Sinusitis - otitis media - pneumonia
Active; passive - fast but short half life (3 weeks!)
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

41. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
In the germinal center of secondary follicles (In the paler center)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
...

42. What is the main function of IL 8?
Active; passive - fast but short half life (3 weeks!)
A chemotactic factor for neutrophils
IgM
Negative!

43. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Anti Jo -1
Internal iliac
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

44. What is a type I hypersensitivity reaction? What is atopic?
...
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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

45. What is the toxicity of azathioprine?
pale central germinal centers
...
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
IgG

46. In thymic development - What is the positive selection? negative selections?
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
When you select for which MHC it will have; take out the lymphs that self react
dimer
NK cells

47. Which cytokines do Th2 release and For what?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

48. What is recomb beta interferon used for?
MS
heavy chains
IL 5
Anti viral and anti tumor

49. What cytokines are released by Th1 cells?
CD56
Interferon gamma and IL 2
Negative!
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

50. What are four results of a splenectomy?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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