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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. hat is the presentation of Jobs syndrome or Hyper IgE?
B - T - and NK cells
Thrombocytopenia
Alternative splicing of mRNA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

2. Which disease is associated withB B27?
T
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Th2; Th1

3. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Activate macrophages

4. What do multimeric antibodies require for assembly?
Anti SS- A (anti RO) and Anti SS- B
Interferon gamma; Th1
A j chain
dimer

5. What is the mechanism for sirolimus? what else it known as?
MHC II - B7
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
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

6. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Axillary
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti smooth muscle

7. What is the presentation of common variable immunodef? and What are the labs?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
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
Activates Th1 helper cells; Macrophages

8. What are the autoantibodies for systemic sclerosis?
Anti Jo -1
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Superficial inguinal
Anti topoisomerase

9. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Anemias (esp due to renal failure)
pathogenesis
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

10. What are the function of B cells?
Carbohydrate
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IL 4 - 5 - 10 - 6
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

11. What are the main symptoms of B cell immunodeficiencies?
Daclizumab; prevent ACUTE rejection of renal transplant
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
SP infections
B - T - and NK cells

12. What happens in a deficiency of C3?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

13. What is the most common example of passive immunity?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgAs in mothers breast milk!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
lowest concentration

14. What are MHC's necessary for? By themselves?
Influenza; antigenic shift; antigenic drift
TLR ad nuclear receptors
T cell activation; no with CD 4 or CD 8
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

15. What does it mean if there are igM in the serum at birth?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
A recomb cytokine of IL 2; RCC and metastatic melanoma
isotype

16. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

17. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Activates cytotoxic CD 8 T cells as second signal
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
opsonizes
pathogenesis

18. where do NK cells develop?
Not thymus - BM
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti smooth muscle
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

19. What are the autoantibodies for autoimmune hepatitis?
SP infections
Anti smooth muscle
Interferon gamma and IL 2
pathogenesis

20. What lymph node drains the upper limb?
Axillary
Superficial inguinal
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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

21. A lymph node is a ________ lymphoid organ.
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!
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
secondary
Influenza; antigenic shift; antigenic drift

22. What are the mediators that mast cells release?
...
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

23. Which antibody mediates immunity to worms? how?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anemias (esp due to renal failure)
IgE; by activating eosinophils
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

24. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
If there is class switching and plasma cell production (that is when memory cells are produced)
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
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

25. What type of side chains are found on Fc region of an antibody?
The igA found in breast milk
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Carbohydrate

26. which antibodies prevent antigens from binding mucosal surfaces?
Anti glutamate carboxylase and anti insulin
IgA
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
CD21 on B cells (although there is T cell lymphocytosis in EBV)

27. Which diseases are associated with DR4?
IgM
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti U1 RNP (ribonucleoprotein)
DM type I and RA

28. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
If there is class switching and plasma cell production (that is when memory cells are produced)
IgM and IgG
Activate macrophages
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

29. What does IL 5 do?
TNF alpha and IL1
Anti smooth muscle
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

30. How is the antigen loaded onto a MHC II?
S. aureus - E. Coli - aspergillus
type four
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
Paracortex; viral infection

31. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
pathogenesis
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

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

33. Which diseases are associated with DR5?
MHC II - B7
IgAs in mothers breast milk!
neutrophilia!
Pernicious Anemia and Hashimotos

34. Which antibodies can be multimeric?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
...
B - T - and NK cells
IgM and IgA

35. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Fc
Inferior mesenteric

36. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
A recomb cytokine of IL 2; RCC and metastatic melanoma
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)

37. How is sirolimus different from tacrolimus?
Lymphocytes
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
opsonizes
If there is class switching and plasma cell production (that is when memory cells are produced)

38. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
CD56
IgE
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Thrombocytopenia

39. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Activates Th1 helper cells; Macrophages
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)
The patient could become cyanotic in the OR!
Popliteal

40. What is the pathology in hyperacute transplant rejection?
Its main effect is a defect in Ab opsonization for killing
Antihistone
Lymphocytes
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

41. The pathogenesis of contact dermatitis is ________ hypersensitivity
T cell dysfunction
C5a
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
type four

42. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

43. What portion of the lymph node is not well developed in DiGeorge Syndrome?
IgG
Its main effect is a defect in Ab opsonization for killing
Histamine; post capillary venules - vasodilation
Paracortex

44. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
B - T - and NK cells
Hemochromatosis

45. What is the presentation of scid? treatment?
IgG
CRP - C3b - IgM
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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

46. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
The patient could become cyanotic in the OR!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

47. What are the autoantibodies for type I diabetes mellitus?
Celiac
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti glutamate carboxylase and anti insulin

48. What are some sinopulmonary infections?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Graves
Influenza; antigenic shift; antigenic drift
Sinusitis - otitis media - pneumonia

49. The MALT/GALT are not...
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
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
encapsulated
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!

50. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Thrombocytopenia
pathogenesis
Anemias (esp due to renal failure)