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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 happens in a deficiency of C1 esterase inhibitor? DAF?
Severe pyogenic infections early in life
CD56
Hereditary angioedema; PNH
Celiac

2. What is the general structure of an Ab?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Anti mitochondrial
2 heavy chains and two light chains
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

3. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
MHC I; from RER with help of the B2 microglobulin
Superficial inguinal
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

4. what ensure that a memory response is generated?
Complement activation (active in both)
Negative selection
If there is class switching and plasma cell production (that is when memory cells are produced)
Interferon gamma and IL 2

5. Only the _______ contribute to the Fc region
Anti IF
pale central germinal centers
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
heavy chains

6. What is recomb gamma interferon used for?
Internal iliac
Hereditary angioedema; PNH
Chronic granulomatous disease
2 heavy chains and two light chains

7. How does complement link innate and adaptive?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
Type IV

8. which antibody activate mast cells - basophils - and eosinophils?
SP infections
Glycoproteins; HLA
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 :(
IgE

9. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgG
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
IgE; by activating eosinophils

10. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
not Ab mediated
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

11. Name two endogenous pyrogens
Paracortex; viral infection
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 1 and IL 6
MHC II - B7

12. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Not thymus - BM
Anti viral and anti tumor
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

13. What are some catalase positive organisms?
Hemochromatosis
In the germinal center of secondary follicles (In the paler center)
S. aureus - E. Coli - aspergillus
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

14. what secretes IL 4?
Basophils! THey want IG E class switch!
IgM
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

15. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
T cell dysfunction
Anemias (esp due to renal failure)

16. What are howell jolly bodies?
Not thymus - BM
MHC I - CD16 - CD56
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

17. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Steroid responsive nephrotic syndrome
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Paracortex

18. The two heavy chains of an antibody contribute to the...
Hereditary angioedema; PNH
Antidote for digoxin intoxication
Fab portion
Paracortex; viral infection

19. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Influenza; antigenic shift; antigenic drift
neutrophilia!
TNF alpha and IL1

20. What cytokines are released by Th1 cells?
Negative nitroblue tetrazolium reduction test
Viral neutralization of igM and IgG!
Interferon gamma and IL 2
Tetanus - Botulinum - HBV - Rabies

21. What is the most common example of passive immunity?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IgAs in mothers breast milk!
Antibody mediated cytotoxicity; either complement dependent or complement independent

22. are Th cells involved in trapping of antigens of endotoxin/LPS?
MHC class molecules bind to KIRS or CD94 to prevent killing
Th cells fail to produce interferon gamma; a lot of IgE
No because no peptide fragment!
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)

23. What is recomb beta interferon used for?
Humoral
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
MS
Immunoflourescent staining of tissue biopsies

24. 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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IgE
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

25. What is immune complex disease? give an example.
Anti viral and anti tumor
neutrophilia!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

26. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Basophils! THey want IG E class switch!
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 Jo -1
IgE

27. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Negative selection
Influenza; antigenic shift; antigenic drift
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
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

28. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IgE; by activating eosinophils

29. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Fab portion
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
IL 4

30. What are the autoantibodies for myasthenia gravis?
Anti alpha subunit 3 of collagen on type IV bm
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti Ach receptor
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

31. What are the autoantibodies for goodpastures syndrome?
Antimicrosomal and antithyroglobulin
Anti alpha subunit 3 of collagen on type IV bm
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

32. What are C1 - C2 - C3 - C4 important for?
...
Viral neutralization of igM and IgG!
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Carbohydrate

33. What is a type I hypersensitivity reaction? What is atopic?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
carboxy terminal
Immunoflourescent staining of tissue biopsies
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

34. what cell surface proteins are on all APCs?
except hyperacute
Hemochromatosis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
MHC II - B7

35. What are the three types of lymphocytes?
Secretory component
active complement pathway
B - T - and NK cells
C5a

36. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Antihistone
Alternative splicing of mRNA
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
Bind FcG for antibody dependent cellular cytotoxicity

37. How do you test for chronic granulomatous disease?
IL 5
Negative nitroblue tetrazolium reduction test
T cell activation; no with CD 4 or CD 8
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

38. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
type four
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

39. What kinds of receptors activate innate immunity?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Carbohydrate
TLR ad nuclear receptors

40. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
carboxy terminal
IgG
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

41. What is an example of a parasite showing antigenic variation?
Popliteal
except hyperacute
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

42. What is the marginal zone of the spleen? what happens there?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
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
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

43. What does granzyme do? who secretes it?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
All MHC 1/CD8
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
Its a serine protease that activates apoptosis; NK and CD8

44. What is hereditary angioedema? What are the C3 levels?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Superficial inguinal
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

45. Name the three opsonins
Cyclosporine - OKT3
No because no peptide fragment!
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)
CRP - C3b - IgM

46. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti glutamate carboxylase and anti insulin
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

47. Type Iv hypersensitivity is...
delayed!
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
MHC I - CD16 - CD56

48. What lymph node drains the scrotum?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Superficial inguinal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

49. What can cause a lymph node enlargement?
IgE
Local infection/inflammation; infection of the ln itself; metastasis
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

50. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Activates Th1 helper cells; Macrophages
Th2; Th1
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!