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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. Which are the only two antiinflammatory cytokines?
TLR ad nuclear receptors
cannot cross placenta
TGF beta and IL 10
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

2. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
type four
Steroid responsive nephrotic syndrome
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

3. Only the _______ contribute to the Fc region
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
The igA found in breast milk
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
heavy chains

4. What are the PALS?
Anti IF
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Thrombocytopenia
Chronic granulomatous disease

5. What is the marginal zone of the spleen? what happens there?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Hereditary angioedema; PNH
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

6. What is recomb beta interferon used for?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
MS
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

7. what results in symptoms of shock in an acute hemolytic transfusion reaction?
T cell precursor
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgG
Recom IL 11; thrombocytopenia

8. What is the white pulp of the spleen?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
The patient could become cyanotic in the OR!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

9. 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?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Bind FcG for antibody dependent cellular cytotoxicity
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

10. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
dimer
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Liver! (they are proteins circulating in the blood)

11. 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
MHC II - B7
Delayed type hypersensitivity
IgM and IgA

12. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Complement activation (active in both)
Histamine; post capillary venules - vasodilation
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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

13. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Pernicious Anemia and Hashimotos

14. What does IL 4 do?
Rheumatic arthritis
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

15. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
TNF alpha and IL1
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Carbohydrate
C5a

16. What lymph node drains the scrotum?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Superficial inguinal
Carbohydrate
C5a

17. Complements are...
neutrophilia!
acute phase reactants
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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)

18. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
S. aureus - E. Coli - aspergillus
Antimicrosomal and antithyroglobulin
Antidesmoglein

19. What are superantigens? give two examples.
When you select for which MHC it will have; take out the lymphs that self react
MS - hay fever - SLE - goodpastures
MHC I - CD16 - CD56
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

20. For which toxins are preformed antibodies (passive) given?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
pentamer
MHC I - CD16 - CD56
Tetanus - Botulinum - HBV - Rabies

21. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Macrophages - Dendritic cells - B cells
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

22. How does igA cross the epithelium?
TGF beta and IL 10
Severe pyogenic infections early in life
By transcytosis
Tetanus - Botulinum - HBV - Rabies

23. which interleukin receptor is required for NK development? activation?
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
Rheumatic arthritis
IL 15; IL 12 - interferon Beta and interferon alpha
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

24. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
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
Edema and necrosis in that region
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

25. Which cytokines do Th2 release and For what?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The patient could become cyanotic in the OR!
Barrel hoop basement membrane fenestrations
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

26. What are the autoantibodies for sjorgens syndrome?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
pathogenesis
T
Anti SS- A (anti RO) and Anti SS- B

27. What are the autoantibodies for primary biliary cirrhosis?
IgE; by activating eosinophils
Anti TSh receptor
Anti mitochondrial
Chronic granulomatous disease

28. How is the antigen loaded onto a MHC II?
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
When you select for which MHC it will have; take out the lymphs that self react
IL 1 and IL 6
Inferior mesenteric

29. what secretes IL 4?
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Basophils! THey want IG E class switch!
IgM and IgG

30. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
A recomb cytokine of IL 2; RCC and metastatic melanoma

31. The lymphocytes are ________ origin
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
mesenchymal
Yes
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

32. What is the clinical use for azathioprine?
Cross link
neutrophilia!
...
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

33. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Humoral
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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

34. Which diseases are associated with DR4?
TNF alpha and IL1
Paracortex; viral infection
DM type I and RA
heavy chains

35. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Superficial inguinal
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
DM type I

36. What lymph node drains the lateral side of the dorsum of the foot?
No because no peptide fragment!
IgM
Popliteal
Th2; Th1

37. ________ regulate the cell mediated response.
Active; passive - fast but short half life (3 weeks!)
Acts as second signal on B cells to induce class switching to IgE and IgG
Humoral
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

38. How fast does it occur?
When you select for which MHC it will have; take out the lymphs that self react
Th cells fail to produce interferon gamma; a lot of IgE
Edema and necrosis in that region
The patient could become cyanotic in the OR!

39. The alternative pathway is the only constutively...
active complement pathway
Cross link
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgM and IgA

40. What is the toxicity of muromonab?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Macrophages - Dendritic cells - B cells
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

41. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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
A chemotactic factor for neutrophils
Cross link

42. when can graft versus host disease? What is the result?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
A j chain
TNF alpha and IL1

43. What is the main cytokine that activates eosinophils?
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 5
Hemochromatosis

44. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

45. What is the pathology in hyperacute transplant rejection?
Chronic granulomatous disease
...
MHC I; from RER with help of the B2 microglobulin
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

46. What is a type I hypersensitivity reaction? What is atopic?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

47. What are the autoantibodies for pemphigus bulgaris?
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
Antidesmoglein
Anti U1 RNP (ribonucleoprotein)
TGF beta and IL 10

48. What are the autoantibodies for other vasculitides?
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!
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
MHC I - CD16 - CD56

49. To what portion of the Antibody do the complements bind?
Pernicious Anemia and Hashimotos
IgG
Fc
Histamine; post capillary venules - vasodilation

50. What lymph node drains the breast?
Axillary
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Intracellular pathogens (acute and chronic viruses and virally induced cancers)