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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 immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 5
Anti Ach receptor

2. which antibodies prevent antigens from binding mucosal surfaces?
The patient could become cyanotic in the OR!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgA
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

3. What are the function of B cells?
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Acts as second signal on B cells to induce class switching to IgE and IgG
active complement pathway

4. ________ regulate the cell mediated response.
Influenza; antigenic shift; antigenic drift
Cytokine IL 10 secreted by Th2
Humoral
heavy chains

5. Which disease is associated with DR7?
Negative selection
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Steroid responsive nephrotic syndrome

6. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Anti glutamate carboxylase and anti insulin
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
heavy chains

7. What is the pathology of acute transplant rejection? is it reversible?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Barrel hoop basement membrane fenestrations
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

8. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Interferon gamma; Th1
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

9. Describe the capsular structure of a lymph node; What are the functions of the LN?
A chemotactic factor for neutrophils
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
TGF beta and IL 10
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

10. What is thrombopoietin used for?
Thrombocytopenia
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
DM type I

11. Which disease is associated with HLA A3?
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
Hemochromatosis
Th cells fail to produce interferon gamma; a lot of IgE
Wiskott Aldrich syndrome

12. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Activate macrophages
neutrophilia!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

13. what cell surface marker is used for NK cells as it is unique to them?
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
CD56
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

14. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Para aortic
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

15. What is the general structure of an Ab?
Immunosuppression after kidney transplantation
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
2 heavy chains and two light chains
Macrophages - Dendritic cells - B cells

16. What is the presentation of Brutons agammaglobulinemia?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
carboxy terminal
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

17. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
Antimicrosomal and antithyroglobulin
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!
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

18. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
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
Histamine; post capillary venules - vasodilation
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

19. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Antimicrosomal and antithyroglobulin
TGF beta and IL 10
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

20. Describe complement dependent Type II hypersensitivity. Give an example.
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
RNA segment reassortment
Th2; Th1
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

21. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
IgAs in mothers breast milk!
All MHC 1/CD8
The igA found in breast milk
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

22. The idiotype; the Fc portion determines the...
TNF alpha and IL1
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti smooth muscle
isotype

23. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
A chemotactic factor for neutrophils
Carbohydrate
Axillary

24. Which type of selection of thymic development provides central tolerance?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Superficial inguinal
Negative selection
IgG

25. Which disease is associated with B8?
Stimulate the liver to release acute phase reactants
Graves
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

26. describe the pathogenesis of delayed type IV hypersensitivity
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Cyclosporine - OKT3
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Th2; Th1

27. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Basophils! THey want IG E class switch!
IgAs in mothers breast milk!
Superficial inguinal

28. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
TLR ad nuclear receptors
Secretory component
IgG
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

29. The lymphocytes are ________ origin
A - B - C; all the D's
IL 4
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
mesenchymal

30. what will NK cells do to cells covered in IgG Ab? why?
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
Yes
Its main effect is a defect in Ab opsonization for killing
Kill them because they have CD16 on them that recognize the FcG portion

31. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Severe pyogenic infections early in life
Antihistone
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)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

32. What type of fenestrations are found in the red pulp of the spleen?
Basophils! THey want IG E class switch!
SP infections
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Barrel hoop basement membrane fenestrations

33. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
delayed!
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Acts as second signal on B cells to induce class switching to IgE and IgG
2 heavy chains and two light chains

34. What is the presentation of scid? treatment?
All MHC 1/CD8
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

35. What lymph node drains the scrotum?
Superficial inguinal
No because no peptide fragment!
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

36. what mediates the type II hypersensitivity? What are the two different methods?
Secretory component
Antibody mediated cytotoxicity; either complement dependent or complement independent
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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

37. How do you test for type III hypersensitivity?
dimer
CRP - C3b - IgM
Immunoflourescent staining of tissue biopsies
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h

38. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

39. Name the three opsonins
Anti Jo -1
CRP - C3b - IgM
Antihistone
T cell dysfunction

40. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

41. What is colostrum?
...
Popliteal
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
The igA found in breast milk

42. What are the cell surface proteins for Macrophages? which two are for opsonins?
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
T
IgM

43. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
IgG
Cross link
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. where are complements produced?
Interferon gamma; Th1
isotype
Liver! (they are proteins circulating in the blood)
Humoral

45. A lymph node is a ________ lymphoid organ.
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
secondary
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

46. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IL 15; IL 12 - interferon Beta and interferon alpha

47. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
isotype

48. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
2 heavy chains and two light chains
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Secretory component

49. To what portion of the Antibody do the complements bind?
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
Viral neutralization of igM and IgG!
Anti U1 RNP (ribonucleoprotein)
Fc

50. Which disease is associated with DR3?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
DM type I
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E