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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 an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
DM type I and RA
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

2. What are the autoantibodies for autoimmune hepatitis?
Sinusitis - otitis media - pneumonia
Anti smooth muscle
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

3. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti mitochondrial
Kill them because they have CD16 on them that recognize the FcG portion
IL 5

4. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
active complement pathway
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antibody mediated cytotoxicity; either complement dependent or complement independent

5. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Recom IL 11; thrombocytopenia
delayed!
mesenchymal

6. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Interferon gamma; Th1
Interferon gamma and IL 2
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 place of T cell diff and maturation; ant mediastinum above heart; yes; 2

7. Which disease is associated with B8?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Graves
Activates cytotoxic CD 8 T cells as second signal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

8. How is i Th1 helper cell inhibited?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Cytokine IL 10 secreted by Th2
DM type I
CD21 on B cells (although there is T cell lymphocytosis in EBV)

9. What lymph node drains the thigh?
Superficial inguinal
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
When you select for which MHC it will have; take out the lymphs that self react
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

10. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
In the germinal center of secondary follicles (In the paler center)
Kill them because they have CD16 on them that recognize the FcG portion
Superficial inguinal
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

11. What are the autoantibodies for primary biliary cirrhosis?
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anti mitochondrial
Severe pyogenic infections early in life

12. which cells have more complete tolerance - B or T cells?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
T
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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

13. 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?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Chronic granulomatous disease
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

14. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
T cell dysfunction
Anti topoisomerase
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

15. What is recomb beta interferon used for?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM
MS

16. What is the clinical use for sirolimus? what should you combine it with?
CRP - C3b - IgM
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

17. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Yes
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
Superficial inguinal
Active; passive - fast but short half life (3 weeks!)

18. What is the pathogenesis of a candida skin test?
Stimulate the liver to release acute phase reactants
Cyclosporine - OKT3
Delayed type hypersensitivity
Anti viral and anti tumor

19. what characterizes an arthus reaction?
RNA segment reassortment
IgG
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Edema and necrosis in that region

20. What are the two signals to kill for 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
DM type I and RA
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Activates cytotoxic CD 8 T cells as second signal

21. What can cause a lymph node enlargement?
TNF alpha and IL1
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Local infection/inflammation; infection of the ln itself; metastasis
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

22. What lymph node drains the duodenum - jejunum?
S. aureus - E. Coli - aspergillus
A j chain
Superior mesenteric
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

23. What is the main cytokine released by T cells? What does it do
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IL 3; supports growth and differentiation of bone marrow stem cells
Anti Ach receptor

24. what cell surface proteins are on all APCs?
MHC II - B7
Antimicrosomal and antithyroglobulin
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

25. What are the autoantibodies for Mixed connective tissue disease?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
A j chain
RNA segment reassortment
Anti U1 RNP (ribonucleoprotein)

26. How do you test for chronic granulomatous disease?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Negative nitroblue tetrazolium reduction test
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

27. Name two endogenous pyrogens
IL 1 and IL 6
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
secondary
isotype

28. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
NK cells
The igA found in breast milk
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

29. What are the PALS?
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
encapsulated

30. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Sinusitis - otitis media - pneumonia
Stimulate the liver to release acute phase reactants
pathogenesis
Secretory component

31. What lymph node drains the sigmoid colon?
Yes
IL 1 and IL 6
Inferior mesenteric
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

32. What are the autoantibodies for systemic sclerosis?
pentamer
Anti topoisomerase
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IgA

33. 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)
Edema and necrosis in that region
A j chain
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

34. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Rheumatic arthritis

35. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
IgAs in mothers breast milk!
2 heavy chains and two light chains
Superficial inguinal
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

36. What does IL 10 do? who is secreted by?
No because no peptide fragment!
The igA found in breast milk
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Liver! (they are proteins circulating in the blood)

37. Which disease is associated with DR7?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IgG
Steroid responsive nephrotic syndrome
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

38. What is the autoantibody for SLE that is nonspecific? Specific?
cannot cross placenta
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Fab portion
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

39. What is the clinical use for azathioprine?
When you select for which MHC it will have; take out the lymphs that self react
...
delayed!
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

40. How fast does it occur?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
The patient could become cyanotic in the OR!
pathogenesis
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

41. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
CRP - C3b - IgM

42. What is a factor that is a predictor for a bad transplantation?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Antidote for digoxin intoxication
secondary
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

43. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Lymphocytes
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

44. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Activates Th1 helper cells; Macrophages
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Axillary

45. which cytokine inhibits TH2 cells? secreted by who?
Pernicious Anemia and Hashimotos
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Interferon gamma; Th1
pathogenesis

46. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IL 5
Increases expression of MHC I and MHC II and also activates NK cells
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

47. What is the pathology seen in chronic transplant rejection?
Anti mitochondrial
Rheumatic arthritis
Not thymus - BM
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

48. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Anti alpha subunit 3 of collagen on type IV bm
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

49. What are the main symptoms of T cell immunodeficiencies?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
pentamer
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

50. What are the three types of APCs?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Macrophages - Dendritic cells - B 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