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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. What is the marginal zone of the spleen? what happens there?
Antidote for digoxin intoxication
Type IV
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

2. What is anergy? why does this occur?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

3. is IgM an opsonizer?
opsonizes
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Negative!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

4. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti Ach receptor
...
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

5. What is recomb beta interferon used for?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgM and IgG
MS
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

6. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
Immunoflourescent staining of tissue biopsies
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
MS

7. What is the mechanism for sirolimus? what else it known as?
MHC II - B7
A chemotactic factor for neutrophils
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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

8. what cell surface marker is used for NK cells as it is unique to them?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cyclosporine - OKT3
CD56
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

9. What are the function of B cells?
IgM and IgG
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IL 1 and IL 6
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

10. Which is the most abundant antibody in blood?
Anti glutamate carboxylase and anti insulin
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

11. What are the major functions of Antibodies?
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
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cross link

12. what characterizes an arthus reaction?
Edema and necrosis in that region
All MHC 1/CD8
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!
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

13. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
No because no peptide fragment!
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

14. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

15. What are superantigens? give two examples.
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 :(
The patient could become cyanotic in the OR!
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

16. How do you test for chronic granulomatous disease?
Anti Ach receptor
Th2; Th1
lowest concentration
Negative nitroblue tetrazolium reduction test

17. Type Iv hypersensitivity is...
Tetanus - Botulinum - HBV - Rabies
A - B - C; all the D's
delayed!
Th2; Th1

18. What are the T cell functions?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

19. What are the autoantibodies for sjorgens syndrome?
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
Activates cytotoxic CD 8 T cells as second signal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti SS- A (anti RO) and Anti SS- B

20. What is the toxicity of azathioprine?
...
Anemias (esp due to renal failure)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
except hyperacute

21. What is the pathogenesis of acute transplant rejection? When does it occur?
Axillary
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti U1 RNP (ribonucleoprotein)

22. when can graft versus host disease? What is the result?
IgA
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
Barrel hoop basement membrane fenestrations
TLR ad nuclear receptors

23. What are the autoantibodies for primary biliary cirrhosis?
Paracortex
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
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
Anti mitochondrial

24. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anemias (esp due to renal failure)
carboxy terminal
Popliteal

25. The alternative pathway is the only constutively...
active complement pathway
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Yes
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

26. What does interferon gamma do? What two type of cells does it attack mostly?
dimer
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
NK cells

27. What are the autoantibodies for pemphigus bulgaris?
Pernicious Anemia and Hashimotos
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Antidesmoglein
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

28. What lymph node drains the thigh?
Superior mesenteric
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
Superficial inguinal
Anti mitochondrial

29. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Basophils! THey want IG E class switch!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Paracortex

30. ________ regulate the cell mediated response.
Lymphocytes
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
Humoral
NK cells

31. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
mesenchymal
C5a
Superficial inguinal

32. What does granulysin do?
A j chain
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Hemochromatosis

33. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
delayed!
Severe pyogenic infections early in life
Superficial inguinal

34. IgE has the ___________ in the serum
Antidesmoglein
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
lowest concentration
2 heavy chains and two light chains

35. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Negative selection
Pernicious Anemia and Hashimotos
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

36. What are the PALS?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
A recomb cytokine of IL 2; RCC and metastatic melanoma
False! B cell class switching requires a second signal

37. What is three common causes of severe combined immunodef? What is the result of all three?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Liver! (they are proteins circulating in the blood)
Anti U1 RNP (ribonucleoprotein)

38. What type of side chains are found on Fc region of an antibody?
Kill them because they have CD16 on them that recognize the FcG portion
Its main effect is a defect in Ab opsonization for killing
Antibody mediated cytotoxicity; either complement dependent or complement independent
Carbohydrate

39. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
carboxy terminal
IgA

40. IgG...
opsonizes
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
carboxy terminal

41. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
Anti topoisomerase
Anti Jo -1
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

42. How does igA cross the epithelium?
CD56
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
By transcytosis

43. What are the symptoms of serum sickness?
Activate macrophages
Superior mesenteric
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

44. which of the transplant rejections is antibody mediated? why does it occur?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
cannot cross placenta
Anti SS- A (anti RO) and Anti SS- B
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

45. What is the pathology in hyperacute transplant rejection?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgA
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Inferior mesenteric

46. Which are the only two antiinflammatory cytokines?
Activates Th1 helper cells; Macrophages
T cell activation; no with CD 4 or CD 8
TGF beta and IL 10
DM type I and RA

47. What is the main function of TNF alpha? How does it do this?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Superficial inguinal
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)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

48. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
C5a
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

49. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Its main effect is a defect in Ab opsonization for killing
Interferon gamma; Th1
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

50. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Internal iliac
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Axillary