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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 digoxin immune Fab used for?
except hyperacute
Th cells fail to produce interferon gamma; a lot of IgE
Antidote for digoxin intoxication
Local infection/inflammation; infection of the ln itself; metastasis

2. Type IV hypersensitivity is i...
not Ab mediated
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
except hyperacute

3. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
CRP - C3b - IgM
Interferon gamma; Th1
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

4. what prevents NK cells from killing normal cells if their default is to kill?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Immunoflourescent staining of tissue biopsies
MHC class molecules bind to KIRS or CD94 to prevent killing
IgG

5. what happens in a deficiency of C1 esterase inhibitor? DAF?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Axillary
Hereditary angioedema; PNH

6. What is serum sickness? give an example.
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

7. What are the main Cell surface proteins on T cells?
Antimicrosomal and antithyroglobulin
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgM and IgG

8. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
lowest concentration
Cross link

9. What are the two signals required for T cells? what happens after?
Not thymus - BM
IL 4 - 5 - 10 - 6
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

10. What are the autoantibodies for wegeners granulomatosis?
Immunosuppression after kidney transplantation
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
pale central germinal centers

11. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
The patient could become cyanotic in the OR!
Negative nitroblue tetrazolium reduction test

12. Which disease is associated with DR7?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
Steroid responsive nephrotic syndrome
MHC I - CD16 - CD56

13. what cell surface proteins are on all APCs?
MHC II - B7
Kill them because they have CD16 on them that recognize the FcG portion
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

14. What is recomb beta interferon used for?
Histamine; post capillary venules - vasodilation
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
Tetanus - Botulinum - HBV - Rabies
MS

15. What are the autoantibodies for pemphigus bulgaris?
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Active; passive - fast but short half life (3 weeks!)
Antidesmoglein

16. What links the adaptive and innate immunity?
Acts as second signal on B cells to induce class switching to IgE and IgG
Complement activation (active in both)
IgE
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

17. What are some catalase positive organisms?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
S. aureus - E. Coli - aspergillus
MHC I - CD16 - CD56
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

18. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
mesenchymal
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
lowest concentration
Paracortex; viral infection

19. How is i Th1 helper cell inhibited?
IL 5
Cytokine IL 10 secreted by Th2
acute phase reactants
Increases expression of MHC I and MHC II and also activates NK cells

20. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
Chronic granulomatous disease

21. What is the late phase reaction of anaphylaxis allergy? what mediates it?
IL 15; IL 12 - interferon Beta and interferon alpha
Secretory component
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)
IL 4

22. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Its a serine protease that activates apoptosis; NK and CD8
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 4

23. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Antibody mediated cytotoxicity; either complement dependent or complement independent

24. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Immunoflourescent staining of tissue biopsies
Superficial inguinal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

25. Leukocyte adhesion defect presents with...
neutrophilia!
Paracortex
Anti alpha subunit 3 of collagen on type IV bm
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

26. What do multimeric antibodies require for assembly?
B - T - and NK cells
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
A j chain
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

27. What does IgA pick up from epithelial cells before being secreted?
Anti IF
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Sinusitis - otitis media - pneumonia
Secretory component

28. What are MHC's necessary for? By themselves?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
T cell activation; no with CD 4 or CD 8

29. From where do cytokines come from?
Internal iliac
IgM and IgA
Local infection/inflammation; infection of the ln itself; metastasis
Lymphocytes

30. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

31. Which is the main antibody that provides passive immunity to infants?
IgG
Kill them because they have CD16 on them that recognize the FcG portion
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

32. What is the pathogenesis of a hypersensitivity reaction?
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Carbohydrate
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

33. What is anergy? why does this occur?
IgM and IgA
carboxy terminal
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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

34. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
acute phase reactants
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
CRP - C3b - IgM
IL 1 and IL 6

35. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
Lymphocytes
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

36. Which disease is associated with DR3?
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
DM type I
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

37. How does igA cross the epithelium?
Delayed type hypersensitivity
IgE; by activating eosinophils
By transcytosis
...

38. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Thrombocytopenia
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Immunosuppression after kidney transplantation

39. What is thrombopoietin used for?
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
Anti Jo -1
Fab portion
Thrombocytopenia

40. are Th cells involved in trapping of antigens of endotoxin/LPS?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
RNA segment reassortment
No because no peptide fragment!
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 :(

41. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
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
Glycoproteins; HLA
Superficial inguinal
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

42. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
S. aureus - E. Coli - aspergillus
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
Graves
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

43. What are the autoantibodies for type I diabetes mellitus?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
MHC II - B7
Anti glutamate carboxylase and anti insulin
MS

44. Give an example of someone who could get hyperacute transplant rejection.
Severe pyogenic infections early in life
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Previous transfusion; pregnant woman whose fetus had paternal antigens
heavy chains

45. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgAs in mothers breast milk!
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

46. give an example of how influenza does a major antigenic shift.
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MS
RNA segment reassortment
Anti TSh receptor

47. What are the autoantibodies for primary biliary cirrhosis?
Anti topoisomerase
If there is class switching and plasma cell production (that is when memory cells are produced)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti mitochondrial

48. What lymph node drains the duodenum - jejunum?
Thrombocytopenia
Superior mesenteric
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
C5a

49. What lymph node drains the stomach?
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
Fc
Celiac
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

50. In thymic development - What is the positive selection? negative selections?
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
Kill them because they have CD16 on them that recognize the FcG portion
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
When you select for which MHC it will have; take out the lymphs that self react