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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 PALS?
dimer
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
lowest concentration
Superficial inguinal

2. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Histamine; post capillary venules - vasodilation
Superficial inguinal
Axillary

3. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
IgA
Popliteal
MHC class molecules bind to KIRS or CD94 to prevent killing

4. What links the adaptive and innate immunity?
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
Complement activation (active in both)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti U1 RNP (ribonucleoprotein)

5. What lymph node drains the stomach?
Axillary
Celiac
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Carbohydrate

6. Which disease is associated with DR3?
Antidesmoglein
Antihistone
Graves
DM type I

7. IgG...
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
pathogenesis
Steroid responsive nephrotic syndrome
opsonizes

8. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
heavy chains
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
TLR ad nuclear receptors
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

9. where are complements produced?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Liver! (they are proteins circulating in the blood)
Interferon gamma and IL 2
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

10. Name two endogenous pyrogens
IL 1 and IL 6
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
lowest concentration

11. What is the presentation of scid? treatment?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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)

12. What type of side chains are found on Fc region of an antibody?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Carbohydrate
A chemotactic factor for neutrophils

13. What are some catalase positive organisms?
Bind FcG for antibody dependent cellular cytotoxicity
...
S. aureus - E. Coli - aspergillus
Wiskott Aldrich syndrome

14. What is an example of a parasite showing antigenic variation?
lowest concentration
delayed!
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cyclosporine - OKT3

15. What are the major functions of Antibodies?
Its main effect is a defect in Ab opsonization for killing
Anti Ach receptor
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

16. which B and T cell disorder presents with specifically low IgM?
except hyperacute
Wiskott Aldrich syndrome
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
Receiving preformed Antibodies

17. which antibodies can bind complement?
Sinusitis - otitis media - pneumonia
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgM and IgG
Anti TSh receptor

18. What lymph node drains the testes?
Para aortic
Antimicrosomal and antithyroglobulin
Lymphocytes
acute phase reactants

19. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Histamine; post capillary venules - vasodilation

20. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
IL 4
except hyperacute
IgG
Hemochromatosis

21. How fast does it occur?
delayed!
acute phase reactants
The patient could become cyanotic in the OR!
Internal iliac

22. What do multimeric antibodies require for assembly?
A j chain
Previous transfusion; pregnant woman whose fetus had paternal antigens
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
False! B cell class switching requires a second signal

23. Complements are...
type four
Increases expression of MHC I and MHC II and also activates NK cells
acute phase reactants
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

24. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
By transcytosis
T cell precursor

25. What are the autoantibodies for pernicious anemia?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anti IF
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

26. What lymph node drains the rectum (above the pectinate line)?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anti topoisomerase
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
Internal iliac

27. What are MHC's necessary for? By themselves?
Fc
Liver! (they are proteins circulating in the blood)
T cell activation; no with CD 4 or CD 8
Complement activation (active in both)

28. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Superficial inguinal
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

29. What does interferon gamma do? What two type of cells does it attack mostly?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Inferior mesenteric
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

30. What does Interferon alpha and beta do? how?
In the germinal center of secondary follicles (In the paler center)
Hemochromatosis
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

31. What lymph node drains the upper limb?
NK cells
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Axillary
Not thymus - BM

32. What does interferon gamma do to be antiviral?
Histamine; post capillary venules - vasodilation
Increases expression of MHC I and MHC II and also activates NK cells
Thrombocytopenia
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

33. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Steroid responsive nephrotic syndrome
Popliteal
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

34. What is epo used for?
The patient could become cyanotic in the OR!
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anemias (esp due to renal failure)

35. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
acute phase reactants
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!
Local infection/inflammation; infection of the ln itself; metastasis

36. What is the main function of interferons?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Para aortic

37. To what portion of the Antibody do the complements bind?
IL 4 - 5 - 10 - 6
Fc
Its main effect is a defect in Ab opsonization for killing
Carbohydrate

38. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Alternative splicing of mRNA
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
SP infections
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

39. What are target cells?
Th2; Th1
Steroid responsive nephrotic syndrome
Bind FcG for antibody dependent cellular cytotoxicity
Cells that stil have weird parts of their membrane that macrophages usually bite off

40. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Antimicrosomal and antithyroglobulin
IL 4
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

41. Describe complement dependent Type II hypersensitivity. Give an example.
Wiskott Aldrich syndrome
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
Antihistone
Humoral

42. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
...
By transcytosis
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

43. What is the pathology in hyperacute transplant rejection?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Superior mesenteric
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

44. The secondary follicles have __________; primary follicles are dense
IgM and IgD
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
pale central germinal centers
Cells that stil have weird parts of their membrane that macrophages usually bite off

45. What is filgrastim and sargramostim? and What is it used for?
Receiving preformed Antibodies
TLR ad nuclear receptors
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Viral neutralization of igM and IgG!

46. when can graft versus host disease? What is the result?
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
Inferior mesenteric
acute phase reactants
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

47. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
neutrophilia!
Humoral

48. What does it mean if there are igM in the serum at birth?
Paracortex; viral infection
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
DM type I
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

49. where do NK cells develop?
Kill them because they have CD16 on them that recognize the FcG portion
CD56
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Not thymus - BM

50. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anti topoisomerase
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
A chemotactic factor for neutrophils