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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 are the mediators that mast cells release?
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
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
lowest concentration
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

2. What is an example of a parasite showing antigenic variation?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IL 4 - 5 - 10 - 6

3. What are the cell surface proteins on NK cells?
IL 5
MHC I - CD16 - CD56
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 :(
Complement activation (active in both)

4. Which diseases are associated with DR4?
The patient could become cyanotic in the OR!
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
T cell precursor
DM type I and RA

5. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

6. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti topoisomerase
TNF alpha and IL1

7. when can graft versus host disease? What is the result?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
carboxy terminal

8. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Immunosuppression after kidney transplantation
Negative selection
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 :(
Recom IL 11; thrombocytopenia

9. What does Interferon alpha and beta do? how?
Sinusitis - otitis media - pneumonia
By transcytosis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

10. To what portion of the Antibody do the complements bind?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Fc
Thrombocytopenia
SP infections

11. What is digoxin immune Fab used for?
pale central germinal centers
Antidote for digoxin intoxication
Anti topoisomerase
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

12. What is the main function of IL 8?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Anti viral and anti tumor
A chemotactic factor for neutrophils
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

13. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Histamine; post capillary venules - vasodilation
Cells that stil have weird parts of their membrane that macrophages usually bite off
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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

14. What is the pathology in hyperacute transplant rejection?
Its a serine protease that activates apoptosis; NK and CD8
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
except hyperacute

15. what secretes IL 4?
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
Basophils! THey want IG E class switch!
heavy chains
Internal iliac

16. The pathogenesis of contact dermatitis is ________ hypersensitivity
not Ab mediated
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Superficial inguinal
type four

17. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Antidesmoglein
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 and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti SS- A (anti RO) and Anti SS- B

18. which antibodies can bind complement?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IgM and IgG
Acts as second signal on B cells to induce class switching to IgE and IgG

19. What are superantigens? give two examples.
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti glutamate carboxylase and anti insulin
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
DM type I

20. Only the _______ contribute to the Fc region
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Macrophages - Dendritic cells - B cells
pale central germinal centers
heavy chains

21. What does IL 5 do?
Paracortex
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

22. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
IL 4
Activate macrophages
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

23. What lymph node drains the lateral side of the dorsum of the foot?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Popliteal
Pernicious Anemia and Hashimotos
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

24. what ensure that a memory response is generated?
Anti smooth muscle
If there is class switching and plasma cell production (that is when memory cells are produced)
Glycoproteins; HLA
Interferon gamma and IL 2

25. What is filgrastim and sargramostim? and What is it used for?
IgM
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
The igA found in breast milk
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

26. What lymph node drains the stomach?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Celiac
Popliteal
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

27. What are the autoantibodies for Celiac disease?
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
Anti IF
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

28. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
A j chain
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Not thymus - BM
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

29. What lymph node drains the rectum (above the pectinate line)?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Fab portion
Recom IL 11; thrombocytopenia
Internal iliac

30. What does IgA pick up from epithelial cells before being secreted?
Inferior mesenteric
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Secretory component
Hemochromatosis

31. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Stimulate the liver to release acute phase reactants
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
All MHC 1/CD8

32. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Remove encapsulated bacateria
Chronic granulomatous disease
Histamine; post capillary venules - vasodilation
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 the antimetabolite precursor of 6 mercaptopurine? What is the result?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
T cell activation; no with CD 4 or CD 8
...

34. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
T
Anti U1 RNP (ribonucleoprotein)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

35. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Cyclosporine - OKT3
S. aureus - E. Coli - aspergillus

36. which of the hypersensitivity reactions is not Ab mediated?
Negative selection
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Cytokine IL 10 secreted by Th2
Type IV

37. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
not Ab mediated
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
C5a

38. which antibody is involved in the primary response or immediate response to an antigen?
MHC class molecules bind to KIRS or CD94 to prevent killing
IgM
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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

39. Which is the main antibody that provides passive immunity to infants?
Kill them because they have CD16 on them that recognize the FcG portion
CD21 on B cells (although there is T cell lymphocytosis in EBV)
...
IgG

40. 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)?
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

41. What kinds of receptors activate innate immunity?
MHC I; from RER with help of the B2 microglobulin
Yes
TLR ad nuclear receptors
A - B - C; all the D's

42. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
IgM and IgA
T cell activation; no with CD 4 or CD 8

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

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44. To what disease do the autoantibodies to IgG (rheumatoid factor)?
not Ab mediated
Rheumatic arthritis
carboxy terminal
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

45. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Internal iliac
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

46. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
Cells that stil have weird parts of their membrane that macrophages usually bite off
IgM
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

47. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Delayed type hypersensitivity
B - T - and NK cells
A recomb cytokine of IL 2; RCC and metastatic melanoma

48. which interleukin receptor is required for NK development? activation?
Barrel hoop basement membrane fenestrations
IL 15; IL 12 - interferon Beta and interferon alpha
IL 4 - 5 - 10 - 6
Anti U1 RNP (ribonucleoprotein)

49. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
IL 15; IL 12 - interferon Beta and interferon alpha
Superficial inguinal
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
Yes

50. what bacteria are a splenectomy patient most susceptible to? why?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Antihistone