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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. Name two endogenous pyrogens
Paracortex; viral infection
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
IL 1 and IL 6

2. describe the pathogenesis of delayed type IV hypersensitivity
MS - hay fever - SLE - goodpastures
IgG
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

3. What is chronic mucocutaneous candidiasis d/t?
mesenchymal
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
T cell dysfunction
Axillary

4. What is the presentation of Brutons agammaglobulinemia?
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
Anti alpha subunit 3 of collagen on type IV bm
Anti Jo -1
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

5. What is the toxicity of muromonab?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 4

6. 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
Cyclosporine - OKT3
neutrophilia!
Receiving preformed Antibodies

7. What links the adaptive and innate immunity?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Complement activation (active in both)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antidote for digoxin intoxication

8. What is a factor that is a predictor for a bad transplantation?
Antihistone
Superficial inguinal
Bind FcG for antibody dependent cellular cytotoxicity
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

9. What are the T cell functions?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Its a serine protease that activates apoptosis; NK and CD8
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Chronic granulomatous disease

10. What are the two signals required for Th1 cells? what happens after then activated?
Hemochromatosis
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Interferon gamma and IL 2

11. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
IL 1 and IL 6
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Internal iliac

12. Which disease is associated with DR7?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Steroid responsive nephrotic syndrome
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Kill them because they have CD16 on them that recognize the FcG portion

13. 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).
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Graves
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
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!

14. What are C1 - C2 - C3 - C4 important for?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Viral neutralization of igM and IgG!
DM type I and RA

15. IgM can exist as a _______ also
Acts as second signal on B cells to induce class switching to IgE and IgG
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
pentamer
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

16. What are the autoantibodies for pemphigus bulgaris?
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 1 and IL 6
Antidesmoglein
Negative nitroblue tetrazolium reduction test

17. What does IL 4 do?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Acts as second signal on B cells to induce class switching to IgE and IgG
Cytokine IL 10 secreted by Th2

18. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Chronic granulomatous disease
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Fc
Anti smooth muscle

19. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
IgAs in mothers breast milk!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

20. what characterizes an arthus reaction?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Graves
Edema and necrosis in that region
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

21. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
SP infections
type four
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

22. Describe the complement independent Type II hypersenstivity reaction. Give an example.
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Fc
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

23. where do somatic hypermutation and class switching occur?
Graves
Thrombocytopenia
In the germinal center of secondary follicles (In the paler center)
Barrel hoop basement membrane fenestrations

24. What lymph node drains the lateral side of the dorsum of the foot?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IL 3; supports growth and differentiation of bone marrow stem cells
TLR ad nuclear receptors
Popliteal

25. What are the symptoms of serum sickness?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

26. What is the presentation of scid? treatment?
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
Acts as second signal on B cells to induce class switching to IgE and IgG
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

27. What is the general structure of an Ab?
Th cells fail to produce interferon gamma; a lot of IgE
Para aortic
2 heavy chains and two light chains
Anti topoisomerase

28. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
S. aureus - E. Coli - aspergillus
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

29. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
pentamer
...
Axillary

30. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
Axillary
Kill them because they have CD16 on them that recognize the FcG portion
A chemotactic factor for neutrophils

31. What lymph node drains the breast?
DM type I and RA
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Axillary
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

32. What is oprelevkin? and What is it used for?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Its a serine protease that activates apoptosis; NK and CD8
IgG
Recom IL 11; thrombocytopenia

33. Which disease is associated with HLA A3?
CD56
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 :(
Hemochromatosis
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

34. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
...
Superficial inguinal

35. what cell surface proteins are on all APCs?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
MHC II - B7
Cells that stil have weird parts of their membrane that macrophages usually bite off
Negative selection

36. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Active; passive - fast but short half life (3 weeks!)
Anti IF
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

37. What is recomb alpha interferon used for?
MHC I; from RER with help of the B2 microglobulin
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
...
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

38. What is the most common selective Ig deficiency? What is the presentation?
type four
DM type I
Antibody mediated cytotoxicity; either complement dependent or complement independent
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

39. What is the mechanism for sirolimus? what else it known as?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Carbohydrate
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

40. other than eat and bite RBCs what else do Macrophages of spleen do>
Influenza; antigenic shift; antigenic drift
RNA segment reassortment
Remove encapsulated bacateria
Not thymus - BM

41. Describe the capsular structure of a lymph node; What are the functions of the LN?
SP infections
C5a
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
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

42. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
A recomb cytokine of IL 2; RCC and metastatic melanoma
Alternative splicing of mRNA

43. What are the autoantibodies for other vasculitides?
lowest concentration
Humoral
...
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

44. What lymph node drains the rectum (above the pectinate line)?
cannot cross placenta
Internal iliac
Negative selection
not Ab mediated

45. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
MHC I - CD16 - CD56
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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

46. where do NK cells develop?
Rheumatic arthritis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Not thymus - BM
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

47. What is the marginal zone of the spleen? what happens there?
isotype
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
False! B cell class switching requires a second signal

48. The Fc region is found on the...
carboxy terminal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
SP infections
T cell precursor

49. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Activates cytotoxic CD 8 T cells as second signal
Lymphocytes
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

50. can igG cross the placenta?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Yes
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
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