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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 is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Not thymus - BM
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Antibody mediated cytotoxicity; either complement dependent or complement independent

2. What is epo used for?
lowest concentration
Anemias (esp due to renal failure)
Viral neutralization of igM and IgG!
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

3. 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
dimer
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

4. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
TNF alpha and IL1

5. What is an example of a parasite showing antigenic variation?
Hereditary angioedema; PNH
type four
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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

6. What is filgrastim and sargramostim? and What is it used for?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

7. What are the cell surface proteins on NK cells?
T
MHC II - B7
MHC I - CD16 - CD56
MS - hay fever - SLE - goodpastures

8. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
Activates cytotoxic CD 8 T cells as second signal
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
Macrophages - Dendritic cells - B cells

9. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

10. What is the presentation of common variable immunodef? and What are the labs?
secondary
Inferior mesenteric
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

11. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Lymphocytes
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Its main effect is a defect in Ab opsonization for killing
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

12. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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 IgG
Paracortex; viral infection

13. What is passive immunity?
IL 4
Receiving preformed Antibodies
pale central germinal centers
dimer

14. What bugs can actually infect the lymph node itself?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Daclizumab; prevent ACUTE rejection of renal transplant
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

15. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
isotype
Thrombocytopenia

16. What does it mean if there are igM in the serum at birth?
IL 1 and IL 6
DM type I
acute phase reactants
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

17. What are the autoantibodies for graves?
T cell precursor
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
Edema and necrosis in that region
Anti TSh receptor

18. What is serum sickness? give an example.
Anti SS- A (anti RO) and Anti SS- B
Influenza; antigenic shift; antigenic drift
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

19. What are the autoantibodies for sjorgens syndrome?
Sinusitis - otitis media - pneumonia
Th2; Th1
Recom IL 11; thrombocytopenia
Anti SS- A (anti RO) and Anti SS- B

20. What do multimeric antibodies require for assembly?
pathogenesis
Anti topoisomerase
A j chain
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

21. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
pale central germinal centers
cannot cross placenta

22. What are the autoantibodies for pernicious anemia?
Anti IF
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Daclizumab; prevent ACUTE rejection of renal transplant

23. What does interferon gamma do to be antiviral?
Stimulate the liver to release acute phase reactants
Increases expression of MHC I and MHC II and also activates NK cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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!

24. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

25. can igG cross the placenta?
Anti glutamate carboxylase and anti insulin
Yes
Anti viral and anti tumor
Local infection/inflammation; infection of the ln itself; metastasis

26. What is recomb gamma interferon used for?
Chronic granulomatous disease
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Liver! (they are proteins circulating in the blood)

27. What is recomb alpha interferon used for?
Antidote for digoxin intoxication
not Ab mediated
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

28. How do you test for chronic granulomatous disease?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
...
Negative nitroblue tetrazolium reduction test
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

29. What is a factor that is a predictor for a bad transplantation?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

30. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Anti Jo -1
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)
False! B cell class switching requires a second signal

31. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Paracortex; viral infection

32. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
NK cells
Sinusitis - otitis media - pneumonia

33. what happens in a deficiency of C1 esterase inhibitor? DAF?
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Sinusitis - otitis media - pneumonia
active complement pathway
Hereditary angioedema; PNH

34. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
A chemotactic factor for neutrophils
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
TLR ad nuclear receptors
Anti viral and anti tumor

35. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgG
...
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

36. what cell surface proteins are on all APCs?
MHC II - B7
Edema and necrosis in that region
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Stimulate the liver to release acute phase reactants

37. What lymph node drains the stomach?
A chemotactic factor for neutrophils
Celiac
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

38. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
Anemias (esp due to renal failure)
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 :(
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)

39. The alternative pathway is the only constutively...
Previous transfusion; pregnant woman whose fetus had paternal antigens
active complement pathway
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Hereditary angioedema; PNH

40. What is the pathogenesis of a candida skin test?
Anti Ach receptor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Delayed type hypersensitivity

41. where do somatic hypermutation and class switching occur?
MHC II - B7
MS
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
In the germinal center of secondary follicles (In the paler center)

42. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
dimer
T cell activation; no with CD 4 or CD 8
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Rheumatic arthritis

43. Only the _______ contribute to the Fc region
Anti Jo -1
MHC I; from RER with help of the B2 microglobulin
Inferior mesenteric
heavy chains

44. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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 :(
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

45. What lymph node drains the thigh?
Daclizumab; prevent ACUTE rejection of renal transplant
Superficial inguinal
isotype
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

46. where do NK cells develop?
Not thymus - BM
cannot cross placenta
Edema and necrosis in that region
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi

47. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
All MHC 1/CD8
Thrombocytopenia
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. Which helper T cells' development is induced by IL 4? IL 12?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Fab portion
Th2; Th1
Rheumatic arthritis

49. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
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
Antidesmoglein
NK cells

50. Complements are...
pathogenesis
heavy chains
Tetanus - Botulinum - HBV - Rabies
acute phase reactants