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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. Complements are...
delayed!
acute phase reactants
Superior mesenteric
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

2. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Humoral
pentamer

3. are Th cells involved in trapping of antigens of endotoxin/LPS?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
No because no peptide fragment!
MS
Not thymus - BM

4. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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 4
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

5. In general What are T cells good for?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti viral and anti tumor
IL 1 and IL 6

6. What lymph node drains the breast?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Axillary
S. aureus - E. Coli - aspergillus
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

7. what cytokine does basophils secrete?
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IL 4

8. What is chronic mucocutaneous candidiasis d/t?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti topoisomerase
IgG
T cell dysfunction

9. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
DM type I and RA

10. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Cross link
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
heavy chains
Activate macrophages

11. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Wiskott Aldrich syndrome
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
encapsulated

12. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Anti TSh receptor
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 :(
except hyperacute
Interferon gamma and IL 2

13. Type IV hypersensitivity is i...
pentamer
not Ab mediated
Type IV
Steroid responsive nephrotic syndrome

14. IgG...
opsonizes
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
MHC I; from RER with help of the B2 microglobulin
CD21 on B cells (although there is T cell lymphocytosis in EBV)

15. A lymph node is a ________ lymphoid organ.
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
dimer
secondary
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

16. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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

17. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Activates Th1 helper cells; Macrophages
The igA found in breast milk
Barrel hoop basement membrane fenestrations

18. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
MHC I; from RER with help of the B2 microglobulin
MHC I - CD16 - CD56
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

19. which antibody activate mast cells - basophils - and eosinophils?
IgE
Activates cytotoxic CD 8 T cells as second signal
A j chain
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

20. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Acts as second signal on B cells to induce class switching to IgE and IgG
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

21. What is hereditary angioedema? What are the C3 levels?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Antidesmoglein

22. How is i Th1 helper cell inhibited?
Local infection/inflammation; infection of the ln itself; metastasis
delayed!
Edema and necrosis in that region
Cytokine IL 10 secreted by Th2

23. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Thrombocytopenia
heavy chains
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
All MHC 1/CD8

24. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Graves
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
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

25. Leukocyte adhesion defect presents with...
All MHC 1/CD8
neutrophilia!
Fc
Immunosuppression after kidney transplantation

26. The lymphocytes are ________ origin
mesenchymal
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
pale central germinal centers
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

27. What are the major functions of Antibodies?
Anti mitochondrial
Hereditary angioedema; PNH
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MHC I; from RER with help of the B2 microglobulin

28. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
When you select for which MHC it will have; take out the lymphs that self react
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

29. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
Chronic granulomatous disease
Local infection/inflammation; infection of the ln itself; metastasis
Anti viral and anti tumor

30. What is digoxin immune Fab used for?
Secretory component
Antidote for digoxin intoxication
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Negative selection

31. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Severe pyogenic infections early in life
IL 1 and IL 6
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

32. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Active; passive - fast but short half life (3 weeks!)
Celiac
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

33. What is the main function of IL 8?
A chemotactic factor for neutrophils
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
heavy chains
The patient could become cyanotic in the OR!

34. What lymph node drains the scrotum?
delayed!
MS - hay fever - SLE - goodpastures
Superficial inguinal
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

35. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Paracortex
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

36. Which diseases are associated with DR4?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
DM type I and RA
IgG
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

37. describe the classic complement pathway.
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

38. What is immune complex disease? give an example.
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Kill them because they have CD16 on them that recognize the FcG portion
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

39. What are four results of a splenectomy?
Glycoproteins; HLA
In the germinal center of secondary follicles (In the paler center)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

40. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
C5a
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

41. what happens in a deficiency of C1 esterase inhibitor? DAF?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Hereditary angioedema; PNH
Superficial inguinal
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

42. what mediates the type II hypersensitivity? What are the two different methods?
MS - hay fever - SLE - goodpastures
Antibody mediated cytotoxicity; either complement dependent or complement independent
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

43. 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
Influenza; antigenic shift; antigenic drift
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
secondary

44. Describe complement dependent Type II hypersensitivity. Give an example.
Glycoproteins; HLA
Anti topoisomerase
Macrophages - Dendritic cells - B cells
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

45. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
carboxy terminal
TNF alpha and IL1
MS

46. What are the autoantibodies for graves?
IL 15; IL 12 - interferon Beta and interferon alpha
Viral neutralization of igM and IgG!
Anti TSh receptor
cannot cross placenta

47. 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!
Severe pyogenic infections early in life
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

48. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Viral neutralization of igM and IgG!
TNF alpha and IL1
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
Previous transfusion; pregnant woman whose fetus had paternal antigens

49. 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!
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Barrel hoop basement membrane fenestrations
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

50. The pathogenesis of contact dermatitis is ________ hypersensitivity
IL 4
If there is class switching and plasma cell production (that is when memory cells are produced)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
type four