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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.
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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 bacteria are a splenectomy patient most susceptible to? why?
...
False! B cell class switching requires a second signal
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
IgAs in mothers breast milk!

2. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
active complement pathway
Activates cytotoxic CD 8 T cells as second signal

3. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

4. what happens in a deficiency of C1 esterase inhibitor? DAF?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Hereditary angioedema; PNH
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti topoisomerase

5. What links the adaptive and innate immunity?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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)
Complement activation (active in both)
A - B - C; all the D's

6. What are the autoantibodies for goodpastures syndrome?
Macrophages - Dendritic cells - B cells
Inferior mesenteric
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti alpha subunit 3 of collagen on type IV bm

7. what results in symptoms of shock in an acute hemolytic transfusion reaction?
MS - hay fever - SLE - goodpastures
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
False! B cell class switching requires a second signal
pale central germinal centers

8. What lymph node drains the sigmoid colon?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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 :(
Inferior mesenteric

9. To what disease do the autoantibodies to IgG (rheumatoid factor)?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Rheumatic arthritis
Stimulate the liver to release acute phase reactants
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. What happens in a secondary follicle?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Bind FcG for antibody dependent cellular cytotoxicity
dimer

11. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Negative!
Axillary
MHC I - CD16 - CD56

12. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Anti viral and anti tumor
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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

13. What lymph node drains the breast?
Chronic granulomatous disease
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Thrombocytopenia
Axillary

14. From where do cytokines come from?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Lymphocytes
Internal iliac

15. The lymphocytes are ________ origin
mesenchymal
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Secretory component

16. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
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

17. Describe the complement independent Type II hypersenstivity reaction. Give an example.
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
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Viral neutralization of igM and IgG!

18. To what portion of the Antibody do the complements bind?
Sinusitis - otitis media - pneumonia
carboxy terminal
Fc
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 ensure that a memory response is generated?
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
pentamer
If there is class switching and plasma cell production (that is when memory cells are produced)
Active; passive - fast but short half life (3 weeks!)

20. which B and T cell disorder presents with specifically low IgM?
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
2 heavy chains and two light chains
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Wiskott Aldrich syndrome

21. What are the autoantibodies for polymyositis and dermatomyositis?
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
Its main effect is a defect in Ab opsonization for killing
Axillary
Anti Jo -1

22. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IL 5
IgAs in mothers breast milk!

23. What are the autoantibodies for autoimmune hepatitis?
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)
Thrombocytopenia
Anti smooth muscle

24. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Active; passive - fast but short half life (3 weeks!)
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

25. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
Immunoflourescent staining of tissue biopsies

26. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti U1 RNP (ribonucleoprotein)
Th2; Th1

27. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
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
T cell dysfunction
Antidesmoglein

28. How is i Th1 helper cell inhibited?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Cytokine IL 10 secreted by Th2
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

29. Only the _______ contribute to the Fc region
heavy chains
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
DM type I

30. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Anti smooth muscle
Delayed type hypersensitivity
Anti IF

31. What is passive immunity?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
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
Receiving preformed Antibodies

32. Which disease is associated with DR3?
pentamer
Th cells fail to produce interferon gamma; a lot of IgE
DM type I
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

33. What lymph node drains the thigh?
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
Superficial inguinal
Active; passive - fast but short half life (3 weeks!)
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx

34. other than eat and bite RBCs what else do Macrophages of spleen do>
Activates cytotoxic CD 8 T cells as second signal
Remove encapsulated bacateria
Influenza; antigenic shift; antigenic drift
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

35. describe the pathogenesis of delayed type IV hypersensitivity
cannot cross placenta
Secretory component
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 cells react to the angtigen and activate leukocyted (macrophage acitivation)

36. What is colostrum?
IgE; by activating eosinophils
The igA found in breast milk
Steroid responsive nephrotic syndrome
Fc

37. What are the autoantibodies for pernicious anemia?
A chemotactic factor for neutrophils
Not thymus - BM
Anti IF
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

38. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti Jo -1
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

39. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Local infection/inflammation; infection of the ln itself; metastasis
encapsulated
Edema and necrosis in that region

40. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
If there is class switching and plasma cell production (that is when memory cells are produced)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Fab portion

41. What lymph node drains the stomach?
MS - hay fever - SLE - goodpastures
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Celiac
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

42. A lymph node is a ________ lymphoid organ.
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
No because no peptide fragment!
secondary

43. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Paracortex; viral infection
Its main effect is a defect in Ab opsonization for killing
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
Activate macrophages

44. which type of immunity is slow but long lasting? as opposed to...
Anti TSh receptor
Active; passive - fast but short half life (3 weeks!)
IL 15; IL 12 - interferon Beta and interferon alpha
Viral neutralization of igM and IgG!

45. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
NK cells
...
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 :(
A j chain

46. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Popliteal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

47. What is anergy? why does this occur?
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
Negative nitroblue tetrazolium reduction test
not Ab mediated
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

48. Which diseases are associated with DR4?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Chronic granulomatous disease
DM type I and RA
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

49. Which disease is associated with HLA A3?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Hemochromatosis
...
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

50. which antibody is involved in the primary response or immediate response to an antigen?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IgM
TNF alpha and IL1
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