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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 lymph node drains the rectum (above the pectinate line)?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
Internal iliac
IgAs in mothers breast milk!

2. __________ are a part of the innate system.
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Popliteal
NK cells
Daclizumab; prevent ACUTE rejection of renal transplant

3. What lymph node drains the duodenum - jejunum?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Barrel hoop basement membrane fenestrations
Superior mesenteric
Rheumatic arthritis

4. 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)?
Antidesmoglein
MS - hay fever - SLE - goodpastures
C5a
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

5. What is the pathology in hyperacute transplant rejection?
Tetanus - Botulinum - HBV - Rabies
Viral neutralization of igM and IgG!
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

6. What is the most common selective Ig deficiency? What is the presentation?
Anti TSh receptor
A chemotactic factor for neutrophils
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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)

7. Which type of selection of thymic development provides central tolerance?
Negative selection
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
DM type I
Fc

8. The two heavy chains of an antibody contribute to the...
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
Immunoflourescent staining of tissue biopsies
Fab portion
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

9. What is the cause of thymic aplasia? What is its presentation? What are the labs?
IgG
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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

10. describe the classic complement pathway.
Steroid responsive nephrotic syndrome
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

11. 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?
encapsulated
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Macrophages - Dendritic cells - B cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

12. What are the main Cell surface proteins on T cells?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Activates cytotoxic CD 8 T cells as second signal
...
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

13. What is recomb beta interferon used for?
T cell precursor
Rheumatic arthritis
MS
A - B - C; all the D's

14. Which is the most abundant antibody in blood?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti viral and anti tumor
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IgG

15. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
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
Pernicious Anemia and Hashimotos
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

16. Describe complement dependent Type II hypersensitivity. Give an example.
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IL 1 and IL 6
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

17. What is the main function of IL 12? other than macrophages who else can release IL 12?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Kill them because they have CD16 on them that recognize the FcG portion
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Yes

18. Which disease is associated with DR7?
lowest concentration
Cross link
Steroid responsive nephrotic syndrome
IgM and IgD

19. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Interferon gamma; Th1
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Receiving preformed Antibodies

20. The ______ in the BM are DN - the DP are in the cortex of thymus
Liver! (they are proteins circulating in the blood)
T cell precursor
pathogenesis
RNA segment reassortment

21. What is Aldesleukin? What is it used for
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
A j chain
A recomb cytokine of IL 2; RCC and metastatic melanoma
Recom IL 11; thrombocytopenia

22. How fast does it occur?
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
The patient could become cyanotic in the OR!
All MHC 1/CD8
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

23. What lymph node drains the scrotum?
MS
RNA segment reassortment
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Superficial inguinal

24. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Alternative splicing of mRNA
IL 1 and IL 6
type four

25. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

26. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Immunoflourescent staining of tissue biopsies
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgA
Type IV

27. How does the alternative pathway lead to MAC activation?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
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
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
Hereditary angioedema; PNH

28. What can cause a lymph node enlargement?
Rheumatic arthritis
Anti SS- A (anti RO) and Anti SS- B
DM type I and RA
Local infection/inflammation; infection of the ln itself; metastasis

29. How does complement link innate and adaptive?
IgAs in mothers breast milk!
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

30. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti mitochondrial

31. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Immunoflourescent staining of tissue biopsies
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

32. Monomer in circulation - ___ when secreted
dimer
B - T - and NK cells
type four
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

33. what mediates the type II hypersensitivity? What are the two different methods?
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
No because no peptide fragment!
Antibody mediated cytotoxicity; either complement dependent or complement independent
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

34. where are complements produced?
Liver! (they are proteins circulating in the blood)
IgE; by activating eosinophils
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

35. What is the clinical use of Muromonab?
IgG
Antihistone
Celiac
Immunosuppression after kidney transplantation

36. The alternative pathway is the only constutively...
Thrombocytopenia
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
active complement pathway
CRP - C3b - IgM

37. What is the main function of interferons?
Steroid responsive nephrotic syndrome
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
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

38. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
DM type I and RA

39. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Axillary
S. aureus - E. Coli - aspergillus
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

40. In general What are T cells good for?
Anti viral and anti tumor
B - T - and NK cells
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
Anti smooth muscle

41. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
SP infections
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
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

42. Give three examples of bacteria that use antigenic variation and how.
delayed!
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IgM and IgD

43. What are the three types of 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
Macrophages - Dendritic cells - B cells
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

44. What are the cell surface proteins on NK cells?
Fc
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Histamine; post capillary venules - vasodilation
MHC I - CD16 - CD56

45. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Celiac
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
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
Acts as second signal on B cells to induce class switching to IgE and IgG

46. What does IL 4 do?
IgG
except hyperacute
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Acts as second signal on B cells to induce class switching to IgE and IgG

47. What are target cells?
MS
A recomb cytokine of IL 2; RCC and metastatic melanoma
Cells that stil have weird parts of their membrane that macrophages usually bite off
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

48. What does CD16 on NK cells do?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
The patient could become cyanotic in the OR!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Bind FcG for antibody dependent cellular cytotoxicity

49. What does interferon gamma do to be antiviral?
secondary
Increases expression of MHC I and MHC II and also activates NK cells
IgE
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

50. What are the labs in brutons agammaglobulinemia?
By transcytosis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Type IV
IgE