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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.
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 does it mean if there are igM in the serum at birth?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
The patient could become cyanotic in the OR!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

2. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
heavy chains
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

3. What can cause a lymph node enlargement?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Local infection/inflammation; infection of the ln itself; metastasis
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

4. In general What are T cells good for?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti viral and anti tumor

5. Which is the most abundant antibody in blood?
2 heavy chains and two light chains
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgG
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)

6. What are the autoantibodies for systemic sclerosis?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti topoisomerase
...
opsonizes

7. What are the mediators that mast cells release?
TLR ad nuclear receptors
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Interferon gamma; Th1
A chemotactic factor for neutrophils

8. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IL 4
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

9. What is the general structure of an Ab?
IgAs in mothers breast milk!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Interferon gamma; Th1
2 heavy chains and two light chains

10. Give three examples of bacteria that use antigenic variation and how.
IgM and IgD
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

11. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Thrombocytopenia
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
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

12. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Macrophages - Dendritic cells - B cells

13. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
DM type I and RA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

14. What are the autoantibodies for autoimmune hepatitis?
Negative!
Chronic granulomatous disease
Anti smooth muscle
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

15. Which diseases are associated with DR4?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
DM type I and RA
Anti smooth muscle
Rheumatic arthritis

16. What are the function of B cells?
Glycoproteins; HLA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Th cells fail to produce interferon gamma; a lot of IgE

17. How do you test for type III hypersensitivity?
isotype
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Severe pyogenic infections early in life
Immunoflourescent staining of tissue biopsies

18. How is sirolimus different from tacrolimus?
T cell precursor
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cross link
pentamer

19. What is the presentation of common variable immunodef? and What are the labs?
Para aortic
RNA segment reassortment
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
Anti SS- A (anti RO) and Anti SS- B

20. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A j chain
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
dimer

21. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
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
IL 5
Remove encapsulated bacateria

22. IgE has the ___________ in the serum
Cells that stil have weird parts of their membrane that macrophages usually bite off
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
lowest concentration
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

23. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
IgM and IgD
heavy chains
Superficial inguinal
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

24. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

25. What is thrombopoietin used for?
Antimicrosomal and antithyroglobulin
Thrombocytopenia
Negative!
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

26. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
Its main effect is a defect in Ab opsonization for killing

27. IgM can fix complement but...
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
cannot cross placenta
Its a serine protease that activates apoptosis; NK and CD8
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

28. What are the three types of lymphocytes?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
CD56
B - T - and NK cells
Kill them because they have CD16 on them that recognize the FcG portion

29. What is the clinical use for sirolimus? what should you combine it with?
Hereditary angioedema; PNH
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Edema and necrosis in that region
Anti Ach receptor

30. 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?
Superficial inguinal
dimer
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
MHC I; from RER with help of the B2 microglobulin

31. Only the _______ contribute to the Fc region
heavy chains
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Paracortex
Negative nitroblue tetrazolium reduction test

32. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Complement activation (active in both)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

33. What lymph node drains the thigh?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Superficial inguinal
Acts as second signal on B cells to induce class switching to IgE and IgG
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

34. What are the labs in brutons agammaglobulinemia?
Wiskott Aldrich syndrome
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Complement activation (active in both)

35. which antibodies can bind complement?
Fab portion
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
Wiskott Aldrich syndrome
IgM and IgG

36. What lymph node drains the sigmoid colon?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Inferior mesenteric

37. What is hereditary angioedema? What are the C3 levels?
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
Superficial inguinal
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

38. What is the main function of interferons?
IgM
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Cross link
Superficial inguinal

39. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
opsonizes
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

40. What is the toxicity of muromonab?
Recom IL 11; thrombocytopenia
IgAs in mothers breast milk!
S. aureus - E. Coli - aspergillus
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

41. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
T

42. How does igA cross the epithelium?
Popliteal
By transcytosis
Activates Th1 helper cells; Macrophages
Basophils! THey want IG E class switch!

43. A lymph node is a ________ lymphoid organ.
secondary
RNA segment reassortment
No because no peptide fragment!
Interferon gamma and IL 2

44. where do somatic hypermutation and class switching occur?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
In the germinal center of secondary follicles (In the paler center)
lowest concentration
MHC class molecules bind to KIRS or CD94 to prevent killing

45. IgG...
opsonizes
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anemias (esp due to renal failure)
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

46. What is colostrum?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The igA found in breast milk
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

47. Which MHC presents intracellular peptides? how so?
MHC I; from RER with help of the B2 microglobulin
delayed!
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
Superficial inguinal

48. What does granzyme do? who secretes it?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anti SS- A (anti RO) and Anti SS- B
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Its a serine protease that activates apoptosis; NK and CD8

49. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Severe pyogenic infections early in life
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Anti SS- A (anti RO) and Anti SS- B

50. The pathogenesis of contact dermatitis is ________ hypersensitivity
Anti Jo -1
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 and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
type four