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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 the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Macrophages - Dendritic cells - B cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

2. IgG...
not Ab mediated
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
opsonizes
Carbohydrate

3. Which disease is associated with DR3?
Receiving preformed Antibodies
DM type I
Antidesmoglein
Basophils! THey want IG E class switch!

4. are Th cells involved in trapping of antigens of endotoxin/LPS?
NK cells
Axillary
Severe pyogenic infections early in life
No because no peptide fragment!

5. What is the pathology seen in chronic transplant rejection?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Viral neutralization of igM and IgG!
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

6. Type IV hypersensitivity is i...
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
not Ab mediated
MHC II - B7
pentamer

7. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
MS - hay fever - SLE - goodpastures
Histamine; post capillary venules - vasodilation
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
Interferon gamma and IL 2

8. which interleukin receptor is required for NK development? activation?
Celiac
S. aureus - E. Coli - aspergillus
IL 15; IL 12 - interferon Beta and interferon alpha
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

9. How is sirolimus different from tacrolimus?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
type four
Antimicrosomal and antithyroglobulin
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

10. What lymph node drains the stomach?
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Celiac
Immunosuppression after kidney transplantation

11. What are the main symptoms of T cell immunodeficiencies?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Interferon gamma; Th1
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti TSh receptor

12. What do multimeric antibodies require for assembly?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
acute phase reactants
cannot cross placenta
A j chain

13. What are the autoantibodies for polymyositis and dermatomyositis?
IgA
Anti Jo -1
NK cells
Paracortex

14. What are superantigens? give two examples.
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Kill them because they have CD16 on them that recognize the FcG portion
TGF beta and IL 10

15. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
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
Local infection/inflammation; infection of the ln itself; metastasis
If there is class switching and plasma cell production (that is when memory cells are produced)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

16. ________ regulate the cell mediated response.
Humoral
Para aortic
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Th cells fail to produce interferon gamma; a lot of IgE

17. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IL 4
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Acts as second signal on B cells to induce class switching to IgE and IgG

18. give an example of how influenza does a major antigenic shift.
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
RNA segment reassortment

19. What cytokines are released by Th1 cells?
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
Interferon gamma and IL 2
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anti U1 RNP (ribonucleoprotein)

20. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
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
IgG
IgE

21. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Histamine; post capillary venules - vasodilation
C5a

22. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Rheumatic arthritis
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Carbohydrate

23. What is filgrastim and sargramostim? and What is it used for?
Anti TSh receptor
By transcytosis
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
...

24. What are the autoantibodies for systemic sclerosis?
IL 4 - 5 - 10 - 6
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti topoisomerase
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

25. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Immunoflourescent staining of tissue biopsies
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

26. is IgM an opsonizer?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Yes
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Negative!

27. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
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
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
TNF alpha and IL1
Anemias (esp due to renal failure)

28. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Axillary
IgM and IgD
lowest concentration
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

29. which antibody is involved in the primary response or immediate response to an antigen?
isotype
IgM
Negative selection
Negative nitroblue tetrazolium reduction test

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

31. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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
DM type I
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

32. What lymph node drains the anal canal (below the pectinate line)?
Interferon gamma; Th1
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Superficial inguinal

33. How fast does it occur?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
The patient could become cyanotic in the OR!

34. What are the autoantibodies for myasthenia gravis?
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti Ach receptor
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

35. What links the adaptive and innate immunity?
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
Complement activation (active in both)
IgA
Type IV

36. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Anti smooth muscle
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

37. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
CRP - C3b - IgM
DM type I and RA
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

38. Describe the Mannose Lectin pathway
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
type four
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

39. What is recomb beta interferon used for?
Delayed type hypersensitivity
IgE; by activating eosinophils
S. aureus - E. Coli - aspergillus
MS

40. To what portion of the Antibody do the complements bind?
Fc
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Hereditary angioedema; PNH
Its a serine protease that activates apoptosis; NK and CD8

41. What is the presentation of hyperIgM syndrome?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
No because no peptide fragment!
Severe pyogenic infections early in life

42. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Histamine; post capillary venules - vasodilation
Internal iliac
Severe pyogenic infections early in life
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

43. What is the pathogenesis of a hypersensitivity reaction?
MHC I - CD16 - CD56
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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

44. What lymph node drains the lateral side of the dorsum of the foot?
In the germinal center of secondary follicles (In the paler center)
DM type I and RA
Popliteal
encapsulated

45. In general What are T cells good for?
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
Anti viral and anti tumor
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

46. hat is the presentation of Jobs syndrome or Hyper IgE?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
MHC I; from RER with help of the B2 microglobulin
The patient could become cyanotic in the OR!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

47. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Anti Ach receptor
Anti smooth muscle

48. Type Iv hypersensitivity is...
Its a serine protease that activates apoptosis; NK and CD8
delayed!
CRP - C3b - IgM
lowest concentration

49. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
T cell precursor
False! B cell class switching requires a second signal

50. What are the autoantibodies for graves?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Sinusitis - otitis media - pneumonia
mesenchymal
Anti TSh receptor