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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 results in symptoms of shock in an acute hemolytic transfusion reaction?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Local infection/inflammation; infection of the ln itself; metastasis
Viral neutralization of igM and IgG!

2. The idiotype; the Fc portion determines the...
Anti smooth muscle
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
isotype
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

3. Type Iv hypersensitivity is...
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Negative selection
delayed!

4. What does it mean if there are igM in the serum at birth?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Superficial inguinal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

5. Which disease is associated with B8?
Graves
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Stimulate the liver to release acute phase reactants
IgA

6. What is anergy? why does this occur?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
DM type I
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

7. What is the autoantibody for SLE that is nonspecific? Specific?
Celiac
B - T - and NK cells
IgG
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

8. Which cytokines do Th2 release and For what?
Negative nitroblue tetrazolium reduction test
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
TGF beta and IL 10
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

9. What is Aldesleukin? What is it used for
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
A recomb cytokine of IL 2; RCC and metastatic melanoma

10. What is the toxicity of azathioprine?
IgG
Anti IF
Viral neutralization of igM and IgG!
...

11. What is the main function of TNF alpha? How does it do this?
Graves
Acts as second signal on B cells to induce class switching to IgE and IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

12. What does Interferon alpha and beta do? how?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
The igA found in breast milk
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

13. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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

14. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Glycoproteins; HLA
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Th2; Th1

15. What lymph node drains the thigh?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Superficial inguinal
Wiskott Aldrich syndrome
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

16. Which disease is associated withB B27?
Anti Ach receptor
Anti U1 RNP (ribonucleoprotein)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

17. What is the presentation of scid? treatment?
opsonizes
IgM and IgD
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Yes

18. What are the three types of APCs?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Macrophages - Dendritic cells - B cells
NK cells
CD56

19. What is the most common example of passive immunity?
Tetanus - Botulinum - HBV - Rabies
Stimulate the liver to release acute phase reactants
Remove encapsulated bacateria
IgAs in mothers breast milk!

20. How does complement link innate and adaptive?
Anti Jo -1
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
Liver! (they are proteins circulating in the blood)

21. The ______ in the BM are DN - the DP are in the cortex of thymus
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
T cell precursor
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

22. What lymph node drains the scrotum?
Superficial inguinal
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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

23. What is the main function of IL 12? other than macrophages who else can release IL 12?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
heavy chains
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!

24. IgM can fix complement but...
cannot cross placenta
lowest concentration
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Kill them because they have CD16 on them that recognize the FcG portion

25. What bugs can actually infect the lymph node itself?
Pernicious Anemia and Hashimotos
Increases expression of MHC I and MHC II and also activates NK cells
Antidesmoglein
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

26. What are the autoantibodies for polymyositis and dermatomyositis?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Anti Jo -1
delayed!
Previous transfusion; pregnant woman whose fetus had paternal antigens

27. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
pale central germinal centers
...

28. What are the autoantibodies for drug induced lupus?
Antihistone
Superficial inguinal
MS
Superior mesenteric

29. 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?
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
When you select for which MHC it will have; take out the lymphs that self react
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
2 heavy chains and two light chains

30. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected 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
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 :(

31. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Local infection/inflammation; infection of the ln itself; metastasis
Cytokine IL 10 secreted by Th2
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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. Give an example of someone who could get hyperacute transplant rejection.
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Delayed type hypersensitivity

33. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
pale central germinal centers
Negative selection
IL 4

34. How fast does it occur?
Type IV
...
Antidote for digoxin intoxication
The patient could become cyanotic in the OR!

35. 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?
Fc
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
Basophils! THey want IG E class switch!
carboxy terminal

36. What is the white pulp of the spleen?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IgE; by activating eosinophils
IL 5

37. What does interferon gamma do? What two type of cells does it attack mostly?
Viral neutralization of igM and IgG!
Secretory component
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Histamine; post capillary venules - vasodilation

38. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
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
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
IgG

39. Describe complement dependent Type II hypersensitivity. Give an example.
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
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
secondary

40. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
Anti mitochondrial
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 :(
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

41. Which is the most abundant antibody in blood?
Superior mesenteric
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgG
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 are the two signals required for T cells? what happens after?
Barrel hoop basement membrane fenestrations
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Graves

43. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Cells that stil have weird parts of their membrane that macrophages usually bite off
Viral neutralization of igM and IgG!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

44. What does IgA pick up from epithelial cells before being secreted?
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
Secretory component
except hyperacute
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

45. What are the autoantibodies for type I diabetes mellitus?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
T
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anti glutamate carboxylase and anti insulin

46. what cell surface proteins are on all APCs?
Antidesmoglein
Rheumatic arthritis
Acts as second signal on B cells to induce class switching to IgE and IgG
MHC II - B7

47. What is passive immunity?
carboxy terminal
Receiving preformed Antibodies
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

48. What are the autoantibodies for graves?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti TSh receptor
False! B cell class switching requires a second signal
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

49. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IgM and IgA
Antihistone
IgA

50. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
pathogenesis
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage