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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. The pathogenesis of contact dermatitis is ________ hypersensitivity
Remove encapsulated bacateria
Increases expression of MHC I and MHC II and also activates NK cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
type four

2. What are the autoantibodies for autoimmune hepatitis?
Anti glutamate carboxylase and anti insulin
IgG
Anti smooth muscle
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

3. Monomer in circulation - ___ when secreted
...
dimer
TLR ad nuclear receptors
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

4. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
NK cells
Internal iliac

5. Describe the capsular structure of a lymph node; What are the functions of the LN?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
The patient could become cyanotic in the OR!
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
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!

6. What is the defect in hyper IgM syndrome? What are the lab results?
Anti mitochondrial
Anti glutamate carboxylase and anti insulin
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
2 heavy chains and two light chains

7. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Immunosuppression after kidney transplantation
Anti glutamate carboxylase and anti insulin

8. What is the presentation of hyperIgM syndrome?
Anti smooth muscle
Severe pyogenic infections early in life
When you select for which MHC it will have; take out the lymphs that self react
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

9. In general What are T cells good for?
Not thymus - BM
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
The patient could become cyanotic in the OR!
Anti viral and anti tumor

10. What is the toxicity of azathioprine?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Complement activation (active in both)
...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

11. IgM can exist as a _______ also
pentamer
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
When you select for which MHC it will have; take out the lymphs that self react
acute phase reactants

12. Which antibody mediates immunity to worms? how?
Anti TSh receptor
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgE; by activating eosinophils
DM type I

13. What type of fenestrations are found in the red pulp of the spleen?
T cell dysfunction
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Barrel hoop basement membrane fenestrations
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

14. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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)
CD56

15. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Th cells fail to produce interferon gamma; a lot of IgE
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Basophils! THey want IG E class switch!

16. What lymph node drains the scrotum?
Influenza; antigenic shift; antigenic drift
Axillary
Superficial inguinal
IgM and IgA

17. What are the autoantibodies for primary biliary cirrhosis?
Activates cytotoxic CD 8 T cells as second signal
Fab portion
Anti mitochondrial
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

18. To what portion of the Antibody do the complements bind?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
isotype
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
Fc

19. What is the most common selective Ig deficiency? What is the presentation?
The patient could become cyanotic in the OR!
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

20. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Influenza; antigenic shift; antigenic drift
Cross link
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

21. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
carboxy terminal
Negative selection
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

22. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Activate macrophages
delayed!

23. In thymic development - What is the positive selection? negative selections?
TGF beta and IL 10
T
When you select for which MHC it will have; take out the lymphs that self react
Acts as second signal on B cells to induce class switching to IgE and IgG

24. which antibody is involved in the primary response or immediate response to an antigen?
T cell activation; no with CD 4 or CD 8
Antimicrosomal and antithyroglobulin
IgM
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

25. What is the treatment of acute transplant rejection?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
pale central germinal centers
Cyclosporine - OKT3

26. What is the autoantibody for SLE that is nonspecific? Specific?
Edema and necrosis in that region
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

27. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

28. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
2 heavy chains and two light chains
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
MHC II - B7

29. Type IV hypersensitivity is i...
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
not Ab mediated
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

30. 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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
...

31. What are the three types of APCs?
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
Macrophages - Dendritic cells - B cells
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
B - T - and NK cells

32. What is the presentation of scid? treatment?
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
Macrophages - Dendritic cells - B cells
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)

33. What is digoxin immune Fab used for?
T cell precursor
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
Antidote for digoxin intoxication

34. which antibodies prevent antigens from binding mucosal surfaces?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgA
IgAs in mothers breast milk!

35. What are the autoantibodies for pernicious anemia?
Anti IF
Increases expression of MHC I and MHC II and also activates NK cells
Lymphocytes
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

36. 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).
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!
Immunosuppression after kidney transplantation
IgG
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

37. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Graves
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
DM type I and RA

38. What is the presentation of common variable immunodef? and What are the labs?
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Edema and necrosis in that region
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

39. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

40. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
SP infections
heavy chains
Hereditary angioedema; PNH

41. What are the autoantibodies for graves?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Increases expression of MHC I and MHC II and also activates NK cells
Anti TSh receptor

42. What is recomb gamma interferon used for?
Chronic granulomatous disease
DM type I and RA
Antihistone
encapsulated

43. Name two endogenous pyrogens
IL 1 and IL 6
IgM and IgA
SP infections
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

44. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
NK cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

45. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Tetanus - Botulinum - HBV - Rabies
Its a serine protease that activates apoptosis; NK and CD8
Antidesmoglein

46. What links the adaptive and innate immunity?
IgM and IgD
Superior mesenteric
Complement activation (active in both)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

47. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

48. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

49. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
not Ab mediated
MHC I - CD16 - CD56
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

50. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Kill them because they have CD16 on them that recognize the FcG portion
pathogenesis
Alternative splicing of mRNA