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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 most common example of passive immunity?
IgAs in mothers breast milk!
Superficial inguinal
False! B cell class switching requires a second signal
lowest concentration

2. What does granulysin do?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

3. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
...
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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

4. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Rheumatic arthritis

5. What is epo used for?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgG
Rheumatic arthritis
Anemias (esp due to renal failure)

6. What is the general structure of an Ab?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
False! B cell class switching requires a second signal
2 heavy chains and two light chains
Internal iliac

7. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Yes
Delayed type hypersensitivity
pale central germinal centers

8. What lymph node drains the duodenum - jejunum?
Superior mesenteric
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
MS
Antibody mediated cytotoxicity; either complement dependent or complement independent

9. Give an example of someone who could get hyperacute transplant rejection.
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
TLR ad nuclear receptors
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Previous transfusion; pregnant woman whose fetus had paternal antigens

10. 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
If there is class switching and plasma cell production (that is when memory cells are produced)
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Anti IF

11. What type of side chains are found on Fc region of an antibody?
IgAs in mothers breast milk!
Carbohydrate
Negative selection
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

12. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activates Th1 helper cells; Macrophages
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
DM type I and RA

13. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Pernicious Anemia and Hashimotos
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Th2; Th1
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 :(

14. Which disease is associated with DR3?
Th cells fail to produce interferon gamma; a lot of IgE
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
DM type I
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

15. what cell surface marker is used for NK cells as it is unique to them?
Barrel hoop basement membrane fenestrations
CD56
MS
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

16. What is the pathogenesis of a hypersensitivity reaction?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
Activates cytotoxic CD 8 T cells as second signal

17. 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)
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
False! B cell class switching requires a second signal

18. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Influenza; antigenic shift; antigenic drift
Wiskott Aldrich syndrome
Cytokine IL 10 secreted by Th2
Superficial inguinal

19. From where do cytokines come from?
S. aureus - E. Coli - aspergillus
Anemias (esp due to renal failure)
Lymphocytes
Paracortex; viral infection

20. What is the pathology of acute transplant rejection? is it reversible?
Antihistone
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
Th cells fail to produce interferon gamma; a lot of IgE

21. Which cytokines do Th2 release and For what?
Influenza; antigenic shift; antigenic drift
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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

22. What are the PALS?
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Anti Ach receptor
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

23. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

24. What is the white pulp of the spleen?
MHC class molecules bind to KIRS or CD94 to prevent killing
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

25. What are the main symptoms of B cell immunodeficiencies?
Anti IF
No because no peptide fragment!
Macrophages - Dendritic cells - B cells
SP infections

26. Only the _______ contribute to the Fc region
RNA segment reassortment
IL 3; supports growth and differentiation of bone marrow stem cells
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
heavy chains

27. IgM can exist as a _______ also
IL 3; supports growth and differentiation of bone marrow stem cells
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
active complement pathway
pentamer

28. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
delayed!
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
A - B - C; all the D's
Cells that stil have weird parts of their membrane that macrophages usually bite off

29. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
If there is class switching and plasma cell production (that is when memory cells are produced)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

30. What is recomb beta interferon used for?
MS
Chronic granulomatous disease
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Macrophages - Dendritic cells - B cells

31. What are MHC's necessary for? By themselves?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
T cell activation; no with CD 4 or CD 8
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

32. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Cytokine IL 10 secreted by Th2

33. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Antihistone
Th cells fail to produce interferon gamma; a lot of IgE
CD56
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

34. How does complement link innate and adaptive?
A - B - C; all the D's
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Complement activation (active in both)
acute phase reactants

35. What lymph node drains the lateral side of the dorsum of the foot?
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
Liver! (they are proteins circulating in the blood)
Popliteal
Cross link

36. What are the two signals required for Th1 cells? what happens after then activated?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
T cell activation; no with CD 4 or CD 8
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

37. What is a type I hypersensitivity reaction? What is atopic?
Paracortex
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Carbohydrate

38. Which type of selection of thymic development provides central tolerance?
Pernicious Anemia and Hashimotos
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Negative selection
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

39. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
A - B - C; all the D's
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

40. What are the main Cell surface proteins on T cells?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
SP infections
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
MHC I; from RER with help of the B2 microglobulin

41. What lymph node drains the scrotum?
Superficial inguinal
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Activates Th1 helper cells; Macrophages
Axillary

42. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Activate macrophages
IgE
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

43. What are the autoantibodies for drug induced lupus?
Delayed type hypersensitivity
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti smooth muscle
Antihistone

44. What are some sinopulmonary infections?
IL 3; supports growth and differentiation of bone marrow stem cells
CD56
Sinusitis - otitis media - pneumonia
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

45. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
CD56
Th2; Th1
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
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

46. What does IL 2 do?
Complement activation (active in both)
Activates cytotoxic CD 8 T cells as second signal
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Th cells fail to produce interferon gamma; a lot of IgE

47. is IgM an opsonizer?
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
Th cells fail to produce interferon gamma; a lot of IgE
IL 1 and IL 6
Negative!

48. what secretes IL 4?
Basophils! THey want IG E class switch!
Wiskott Aldrich syndrome
Antihistone
Bind FcG for antibody dependent cellular cytotoxicity

49. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
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

50. What is the presentation of scid? treatment?
IL 3; supports growth and differentiation of bone marrow stem cells
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Antibody mediated cytotoxicity; either complement dependent or complement independent
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization