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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. Which type of selection of thymic development provides central tolerance?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Negative!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Negative selection

2. describe the pathogenesis of delayed type IV hypersensitivity
By transcytosis
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
MHC I - CD16 - CD56
Celiac

3. Which is the main antibody in the delayed or secondary response to an antigen?
False! B cell class switching requires a second signal
TNF alpha and IL1
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

4. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
When you select for which MHC it will have; take out the lymphs that self react
Alternative splicing of mRNA
dimer

5. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Interferon gamma; Th1
pale central germinal centers
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
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

6. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgE
Acts as second signal on B cells to induce class switching to IgE and IgG
Antimicrosomal and antithyroglobulin

7. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

8. What is filgrastim and sargramostim? and What is it used for?
Anti mitochondrial
dimer
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Immunoflourescent staining of tissue biopsies

9. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
MS
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
MHC class molecules bind to KIRS or CD94 to prevent killing

10. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
encapsulated
Paracortex; viral infection

11. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Stimulate the liver to release acute phase reactants
TNF alpha and IL1
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

12. What is colostrum?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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 igA found in breast milk
Thrombocytopenia

13. What is epo used for?
Anemias (esp due to renal failure)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti Jo -1
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

14. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
Cross link
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Axillary

15. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
When you select for which MHC it will have; take out the lymphs that self react
MHC II - B7
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

16. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
IgE; by activating eosinophils
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
not Ab mediated
Anti SS- A (anti RO) and Anti SS- B

17. What lymph node drains the breast?
Anti smooth muscle
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Its a serine protease that activates apoptosis; NK and CD8
Axillary

18. where do NK cells develop?
Not thymus - BM
Humoral
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

19. which type of immunity is slow but long lasting? as opposed to...
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Celiac
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
Active; passive - fast but short half life (3 weeks!)

20. What are the autoantibodies for goodpastures syndrome?
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
Anti alpha subunit 3 of collagen on type IV bm
IgAs in mothers breast milk!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

21. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

22. The lymphocytes are ________ origin
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
mesenchymal
IgG
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

23. which antibodies can bind complement?
IgM and IgG
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
dimer
MHC II - B7

24. can igG cross the placenta?
Yes
IgM and IgA
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

25. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
IL 3; supports growth and differentiation of bone marrow stem cells
Hemochromatosis
Negative!
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a

26. The secondary follicles have __________; primary follicles are dense
Anti topoisomerase
MHC class molecules bind to KIRS or CD94 to prevent killing
pale central germinal centers
IgAs in mothers breast milk!

27. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Superior mesenteric
encapsulated
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

28. What are the autoantibodies for type I diabetes mellitus?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Anti glutamate carboxylase and anti insulin
Daclizumab; prevent ACUTE rejection of renal transplant
type four

29. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

30. What do multimeric antibodies require for assembly?
A j chain
Steroid responsive nephrotic syndrome
Hereditary angioedema; PNH
Bind FcG for antibody dependent cellular cytotoxicity

31. What is muromonab - CD3 (OKT3)
Bind FcG for antibody dependent cellular cytotoxicity
The igA found in breast milk
Para aortic
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

32. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Daclizumab; prevent ACUTE rejection of renal transplant
IgAs in mothers breast milk!
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)
Anti Ach receptor

33. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Alternative splicing of mRNA
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IL 3; supports growth and differentiation of bone marrow stem cells
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

34. A lymph node is a ________ lymphoid organ.
SP infections
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
DM type I
secondary

35. What are the two signals required for B cell class switching? Which is the second signal?
...
Superior mesenteric
...
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

36. How does igA cross the epithelium?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
By transcytosis
IL 15; IL 12 - interferon Beta and interferon alpha
CD21 on B cells (although there is T cell lymphocytosis in EBV)

37. What lymph node drains the stomach?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Celiac
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
RNA segment reassortment

38. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti mitochondrial
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

39. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
A j chain
Inferior mesenteric
Basophils! THey want IG E class switch!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

40. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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 :(
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

41. Which HLA's are included in MHC I? MHC II?

42. What is the main function of IL 8?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A chemotactic factor for neutrophils
NK cells
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

43. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
TLR ad nuclear receptors
opsonizes
Active; passive - fast but short half life (3 weeks!)
Daclizumab; prevent ACUTE rejection of renal transplant

44. What is passive immunity?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Receiving preformed Antibodies
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

45. What are the autoantibodies for pemphigus bulgaris?
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
Local infection/inflammation; infection of the ln itself; metastasis
Antidesmoglein
Antimicrosomal and antithyroglobulin

46. How is the antigen loaded onto a MHC II?
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
Activates cytotoxic CD 8 T cells as second signal
Antidote for digoxin intoxication
Th cells fail to produce interferon gamma; a lot of IgE

47. Which disease is associated with DR7?
T cell dysfunction
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Steroid responsive nephrotic syndrome

48. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Celiac
IgG

49. What are the autoantibodies for systemic sclerosis?
pale central germinal centers
cannot cross placenta
Anti topoisomerase
Receiving preformed Antibodies

50. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
In the germinal center of secondary follicles (In the paler center)
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
IgG