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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 recomb beta interferon used for?
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
MS
All MHC 1/CD8
Edema and necrosis in that region

2. IgE has the ___________ in the serum
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
If there is class switching and plasma cell production (that is when memory cells are produced)
lowest concentration

3. Which antibody mediates immunity to worms? how?
DM type I and RA
IgE; by activating eosinophils
pale central germinal centers
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

4. What is a factor that is a predictor for a bad transplantation?
Popliteal
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Anti glutamate carboxylase and anti insulin
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

5. What are C1 - C2 - C3 - C4 important for?
Negative nitroblue tetrazolium reduction test
SP infections
Viral neutralization of igM and IgG!
Antidote for digoxin intoxication

6. What is chronic mucocutaneous candidiasis d/t?
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
T cell dysfunction
Complement activation (active in both)
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

7. What is the white pulp of the spleen?
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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)
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

8. T/F B cells do not require a second signal
Tetanus - Botulinum - HBV - Rabies
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
False! B cell class switching requires a second signal
Glycoproteins; HLA

9. what bacteria are a splenectomy patient most susceptible to? why?
Para aortic
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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

10. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
IL 4
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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 :(

11. What is recomb alpha interferon used for?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Activates Th1 helper cells; Macrophages

12. What is thrombopoietin used for?
IL 15; IL 12 - interferon Beta and interferon alpha
S. aureus - E. Coli - aspergillus
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
Thrombocytopenia

13. What are the autoantibodies for drug induced lupus?
Antihistone
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

14. which cells have more complete tolerance - B or T cells?
T
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

15. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
...
Not thymus - BM
C5a
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

16. What are the three types of lymphocytes?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
B - T - and NK cells
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 :(
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

17. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Chronic granulomatous disease
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
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!
MS

18. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti smooth muscle
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

19. what prevents NK cells from killing normal cells if their default is to kill?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
All MHC 1/CD8
Thrombocytopenia
MHC class molecules bind to KIRS or CD94 to prevent killing

20. What is the main function of TNF alpha? How does it do this?
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
IgE; by activating eosinophils
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

21. What is colostrum?
The igA found in breast milk
Basophils! THey want IG E class switch!
The patient could become cyanotic in the OR!
Popliteal

22. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
Its main effect is a defect in Ab opsonization for killing
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
Local infection/inflammation; infection of the ln itself; metastasis

23. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
...
Histamine; post capillary venules - vasodilation
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
secondary

24. Name 5 ways Antibody diversity is generated?
By transcytosis
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
pathogenesis

25. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation

26. What do mature naive B lymphocytes express?
Bind FcG for antibody dependent cellular cytotoxicity
Internal iliac
Macrophages - Dendritic cells - B cells
IgM and IgD

27. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
DM type I and RA
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Cells that stil have weird parts of their membrane that macrophages usually bite off

28. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
...
dimer
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
DM type I and RA

29. when can graft versus host disease? What is the result?
IL 1 and IL 6
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

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

31. What is three common causes of severe combined immunodef? What is the result of all three?
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Th2; Th1
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

32. What is the most common selective Ig deficiency? What is the presentation?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Secretory component
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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

33. What is the pathology seen in chronic transplant rejection?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

34. What does it mean if there are igM in the serum at birth?
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
Anti alpha subunit 3 of collagen on type IV bm
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

35. What is anergy? why does this occur?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgM and IgG
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

36. Name two endogenous pyrogens
IL 1 and IL 6
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti mitochondrial
pale central germinal centers

37. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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!
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)
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
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

38. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Remove encapsulated bacateria
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

39. 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)
Anemias (esp due to renal failure)
Its main effect is a defect in Ab opsonization for killing
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

40. 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?
secondary
Anti smooth muscle
Wiskott Aldrich syndrome
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

41. What are the main symptoms of T cell immunodeficiencies?
IL 4
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
MHC II - B7
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

42. Which is the main antibody that provides passive immunity to infants?
T cell activation; no with CD 4 or CD 8
CD56
IgG
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

43. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
TGF beta and IL 10
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

44. Describe the capsular structure of a lymph node; What are the functions of the LN?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
...

45. What can cause a lymph node enlargement?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Popliteal
Complement activation (active in both)
Local infection/inflammation; infection of the ln itself; metastasis

46. what cytokine does basophils secrete?
IL 4
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

47. A lymph node is a ________ lymphoid organ.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgE
Daclizumab; prevent ACUTE rejection of renal transplant
secondary

48. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Active; passive - fast but short half life (3 weeks!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Paracortex

49. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
2 heavy chains and two light chains
Interferon gamma and IL 2

50. What lymph node drains the breast?
Antihistone
Axillary
IgE; by activating eosinophils
Liver! (they are proteins circulating in the blood)