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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 mediates the type II hypersensitivity? What are the two different methods?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antibody mediated cytotoxicity; either complement dependent or complement independent

2. What can cause a lymph node enlargement?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Liver! (they are proteins circulating in the blood)
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
Local infection/inflammation; infection of the ln itself; metastasis

3. The ______ in the BM are DN - the DP are in the cortex of thymus
DM type I
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
T cell precursor
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

4. What is three common causes of severe combined immunodef? What is the result of all three?
Paracortex
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

5. The MALT/GALT are not...
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Local infection/inflammation; infection of the ln itself; metastasis
encapsulated
DM type I

6. What are the three types of lymphocytes?
T cell activation; no with CD 4 or CD 8
B - T - and NK cells
carboxy terminal
Fab portion

7. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
opsonizes
Paracortex; viral infection

8. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Th2; Th1
IL 5

9. What is the presentation of common variable immunodef? and What are the labs?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgG
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

10. Which disease is associated with DR3?
Fab portion
SP infections
DM type I
Immunosuppression after kidney transplantation

11. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
type four
Anti alpha subunit 3 of collagen on type IV bm
B - T - and NK cells
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

12. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Anti IF
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

13. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
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
Immunoflourescent staining of tissue biopsies
active complement pathway

14. which B and T cell disorder presents with specifically low IgM?
Immunoflourescent staining of tissue biopsies
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Stimulate the liver to release acute phase reactants
Wiskott Aldrich syndrome

15. what secretes IL 4?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Superficial inguinal
Basophils! THey want IG E class switch!
CD56

16. which cytokine inhibits TH2 cells? secreted by who?
IgA
Interferon gamma; Th1
Anti alpha subunit 3 of collagen on type IV bm
Internal iliac

17. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Alternative splicing of mRNA
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 :(
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

18. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
opsonizes
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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

19. What is the treatment of acute transplant rejection?
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)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Cyclosporine - OKT3
Axillary

20. Only the _______ contribute to the Fc region
Negative!
MHC I - CD16 - CD56
heavy chains
Cyclosporine - OKT3

21. What are the autoantibodies for primary biliary cirrhosis?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
isotype
Anti mitochondrial
Remove encapsulated bacateria

22. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antidote for digoxin intoxication
IgM and IgD

23. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide 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
Edema and necrosis in that region
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

24. What does granzyme do? who secretes it?
Increases expression of MHC I and MHC II and also activates NK cells
Lymphocytes
Its a serine protease that activates apoptosis; NK and CD8
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

25. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
Axillary
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

26. describe the pathogenesis of delayed type IV hypersensitivity
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Basophils! THey want IG E class switch!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
not Ab mediated

27. Name the three opsonins
CRP - C3b - IgM
DM type I and RA
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
pale central germinal centers

28. Describe the Mannose Lectin pathway
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

29. What is the main function of interferons?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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)
opsonizes

30. So antibodies are the effectors for the humoral response. List some of their functions.
Anti IF
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
TNF alpha and IL1

31. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Interferon gamma; Th1
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Cross link

32. 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)
By transcytosis
Anti Ach receptor
pathogenesis

33. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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

34. What does IgA pick up from epithelial cells before being secreted?
TGF beta and IL 10
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
The igA found in breast milk
Secretory component

35. which antibodies can bind complement?
Anti TSh receptor
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgM and IgG
Lymphocytes

36. What is recomb beta interferon used for?
IgG
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
MS
mesenchymal

37. can igG cross the placenta?
Yes
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Barrel hoop basement membrane fenestrations
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

38. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
opsonizes
Superficial inguinal
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

39. What does interferon gamma do to be antiviral?
Popliteal
Wiskott Aldrich syndrome
Activates cytotoxic CD 8 T cells as second signal
Increases expression of MHC I and MHC II and also activates NK cells

40. What lymph node drains the sigmoid colon?
S. aureus - E. Coli - aspergillus
Anti Jo -1
Th cells fail to produce interferon gamma; a lot of IgE
Inferior mesenteric

41. What lymph node drains the anal canal (below the pectinate line)?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Superficial inguinal
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

42. Type IV hypersensitivity is i...
A - B - C; all the D's
A recomb cytokine of IL 2; RCC and metastatic melanoma
not Ab mediated
IgM

43. What is the clinical use of Muromonab?
MHC I; from RER with help of the B2 microglobulin
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgA
Immunosuppression after kidney transplantation

44. 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?
Cross link
IgM and IgA
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 15; IL 12 - interferon Beta and interferon alpha

45. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Antihistone
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Cyclosporine - OKT3

46. What is passive immunity?
Antihistone
Cyclosporine - OKT3
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
Receiving preformed Antibodies

47. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Type IV
Antihistone
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

48. A lymph node is a ________ lymphoid organ.
Cross link
T cell precursor
secondary
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

49. Which disease is associated with B8?
When you select for which MHC it will have; take out the lymphs that self react
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Superior mesenteric
Graves

50. What is the general structure of an Ab?
2 heavy chains and two light chains
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Anemias (esp due to renal failure)
encapsulated