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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.
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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 the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
No because no peptide fragment!
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

2. Which disease is associated with HLA A3?
Hemochromatosis
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
isotype
Cyclosporine - OKT3

3. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
encapsulated
Wiskott Aldrich syndrome
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

4. What is the main function of IL 8?
IgA
Antihistone
A chemotactic factor for neutrophils
Axillary

5. which interleukin receptor is required for NK development? activation?
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
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
IL 15; IL 12 - interferon Beta and interferon alpha
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

6. The alternative pathway is the only constutively...
active complement pathway
NK cells
C5a
Anemias (esp due to renal failure)

7. 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?
A - B - C; all the D's
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Graves

8. What is a type I hypersensitivity reaction? What is atopic?
Activates cytotoxic CD 8 T cells as second signal
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

9. What cytokines are released by Th1 cells?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
In the germinal center of secondary follicles (In the paler center)
Interferon gamma and IL 2

10. What are the autoantibodies for myasthenia gravis?
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
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
Anti Ach 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 :(

11. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Activate macrophages
IgM and IgD
The igA found in breast milk

12. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
TLR ad nuclear receptors

13. What are the cell surface proteins on NK cells?
Acts as second signal on B cells to induce class switching to IgE and IgG
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
MHC I - CD16 - CD56
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

14. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Anti topoisomerase
TNF alpha and IL1
Th cells fail to produce interferon gamma; a lot of IgE
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

15. What bugs can actually infect the lymph node itself?
...
opsonizes
Secretory component
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

16. What is the clinical use for sirolimus? what should you combine it with?
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Cytokine IL 10 secreted by Th2

17. What is muromonab - CD3 (OKT3)
Local infection/inflammation; infection of the ln itself; metastasis
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Not thymus - BM
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

18. What is passive immunity?
Receiving preformed Antibodies
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

19. The idiotype; the Fc portion determines the...
Anti Jo -1
By transcytosis
isotype
CD56

20. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Glycoproteins; HLA
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!
Hereditary angioedema; PNH
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

21. What do mature naive B lymphocytes express?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
IgM and IgD
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

22. What does it mean if there are igM in the serum at birth?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
MHC I; from RER with help of the B2 microglobulin
isotype
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

23. What does IgA pick up from epithelial cells before being secreted?
Secretory component
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
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
Acts as second signal on B cells to induce class switching to IgE and IgG

24. Which disease is associated with DR7?
Paracortex; viral infection
Steroid responsive nephrotic syndrome
Liver! (they are proteins circulating in the blood)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

25. 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?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IgA
carboxy terminal
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

26. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Hereditary angioedema; PNH
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

27. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Axillary
IgE; by activating eosinophils
carboxy terminal
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

28. What is digoxin immune Fab used for?
Steroid responsive nephrotic syndrome
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
neutrophilia!
Antidote for digoxin intoxication

29. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
IgG
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
except hyperacute

30. What type of fenestrations are found in the red pulp of the spleen?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Barrel hoop basement membrane fenestrations
MS
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

31. What are the autoantibodies for autoimmune hepatitis?
Axillary
IgA
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti smooth muscle

32. when can graft versus host disease? What is the result?
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
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

33. What is recomb gamma interferon used for?
Negative selection
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Fc
Chronic granulomatous disease

34. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Thrombocytopenia
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
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

35. What are the two signals required for B cell class switching? Which is the second signal?
carboxy terminal
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
T

36. How do you test for chronic granulomatous disease?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Negative nitroblue tetrazolium reduction test
Anti IF
except hyperacute

37. other than C3a - what other complement acts as an anaphyloxin?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
C5a
Active; passive - fast but short half life (3 weeks!)
Yes

38. What is colostrum?
The igA found in breast milk
...
IgM and IgD
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

39. IgE has the ___________ in the serum
lowest concentration
Recom IL 11; thrombocytopenia
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
...

40. What is the pathogenesis of a candida skin test?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Antimicrosomal and antithyroglobulin
Delayed type hypersensitivity

41. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Activates Th1 helper cells; Macrophages

42. Which disease is associated with DR3?
S. aureus - E. Coli - aspergillus
Activate macrophages
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
DM type I

43. What are superantigens? give two examples.
A - B - C; all the D's
Severe pyogenic infections early in life
Steroid responsive nephrotic syndrome
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

44. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
NK cells
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
B - T - and NK 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

45. Which is the most abundant antibody in blood?
IgG
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
False! B cell class switching requires a second signal

46. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Activate macrophages
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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

47. 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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IL 4 - 5 - 10 - 6

48. what cell surface proteins are on all APCs?
IgE; by activating eosinophils
IL 1 and IL 6
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MHC II - B7

49. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Liver! (they are proteins circulating in the blood)

50. What are howell jolly bodies?
Viral neutralization of igM and IgG!
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
dimer
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages