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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 lymph node drains the rectum (above the pectinate line)?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Internal iliac
Negative nitroblue tetrazolium reduction test
encapsulated

2. 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?
active complement pathway
DM type I and RA
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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

3. Describe the capsular structure of a lymph node; What are the functions of the LN?
Recom IL 11; thrombocytopenia
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

4. hat is the presentation of Jobs syndrome or Hyper IgE?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Carbohydrate
Interferon gamma and IL 2
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

5. What lymph node drains the stomach?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Celiac
Inferior mesenteric

6. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Paracortex; viral infection

7. What is the pathogenesis of HyperIgE syndrome? What are the labs?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The igA found in breast milk
Th cells fail to produce interferon gamma; a lot of IgE
Anti topoisomerase

8. which of the hypersensitivity reactions is not Ab mediated?
Barrel hoop basement membrane fenestrations
Type IV
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

9. What is thrombopoietin used for?
Basophils! THey want IG E class switch!
Thrombocytopenia
Recom IL 11; thrombocytopenia
Glycoproteins; HLA

10. What is serum sickness? give an example.
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
IgM and IgA
MHC class molecules bind to KIRS or CD94 to prevent killing
T cell dysfunction

11. 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)?
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
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
Local infection/inflammation; infection of the ln itself; metastasis
Antimicrosomal and antithyroglobulin

12. describe the classic complement pathway.
TGF beta and IL 10
Complement activation (active in both)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

13. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Negative selection
Its main effect is a defect in Ab opsonization for killing
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

14. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
T
All MHC 1/CD8
Its a serine protease that activates apoptosis; NK and CD8
Rheumatic arthritis

15. Type IV hypersensitivity is i...
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Barrel hoop basement membrane fenestrations
not Ab mediated
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

16. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
mesenchymal
type four

17. 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?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
In the germinal center of secondary follicles (In the paler center)
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

18. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
pathogenesis
Negative selection

19. What is muromonab - CD3 (OKT3)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

20. What does granzyme do? who secretes it?
Recom IL 11; thrombocytopenia
Its a serine protease that activates apoptosis; NK and CD8
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

21. 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)
IL 4
T cell precursor
Anti Jo -1

22. What are the major functions of Antibodies?
Viral neutralization of igM and IgG!
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 patient could become cyanotic in the OR!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

23. Which diseases are associated with DR5?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Pernicious Anemia and Hashimotos
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
Anti mitochondrial

24. __________ are a part of the innate system.
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Th cells fail to produce interferon gamma; a lot of IgE
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
NK cells

25. What lymph node drains the anal canal (below the pectinate line)?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Its a serine protease that activates apoptosis; NK and CD8
Yes
Superficial inguinal

26. What is recomb gamma interferon used for?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Chronic granulomatous disease
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
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

27. What kinds of receptors activate innate immunity?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
TLR ad nuclear receptors
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

28. What is the main function of IL 8?
A chemotactic factor for neutrophils
Internal iliac
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

29. What lymph node drains the breast?
Anti smooth muscle
Axillary
S. aureus - E. Coli - aspergillus
Acts as second signal on B cells to induce class switching to IgE and IgG

30. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti IF

31. What is the pathogenesis of a hypersensitivity reaction?
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
TLR ad nuclear receptors
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

32. what mediates the type II hypersensitivity? What are the two different methods?
False! B cell class switching requires a second signal
IgG
Antibody mediated cytotoxicity; either complement dependent or complement independent
Remove encapsulated bacateria

33. What are the main Cell surface proteins on T cells?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgG

34. What are the autoantibodies for autoimmune hepatitis?
Delayed type hypersensitivity
Carbohydrate
Anti smooth muscle
isotype

35. in which immunodef order do you see a lot of pus? no pus?
SP infections
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
CD56
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

36. What is the marginal zone of the spleen? what happens there?
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
DM type I and RA
Active; passive - fast but short half life (3 weeks!)
IL 4 - 5 - 10 - 6

37. which antibody is involved in the primary response or immediate response to an antigen?
IL 3; supports growth and differentiation of bone marrow stem cells
IgM
Sinusitis - otitis media - pneumonia
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

38. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

39. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
No because no peptide fragment!
carboxy terminal
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

40. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
active complement pathway
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Superficial inguinal

41. What are the autoantibodies for hashimotos?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Antimicrosomal and antithyroglobulin
Para aortic
Inferior mesenteric

42. 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
Humoral
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
secondary

43. 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
Anti alpha subunit 3 of collagen on type IV bm
SP infections
acute phase reactants

44. Which disease is associated with DR3?
DM type I
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Fc
Axillary

45. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
Paracortex; viral infection
Activates cytotoxic CD 8 T cells as second signal
Sinusitis - otitis media - pneumonia

46. What lymph node drains the upper limb?
Liver! (they are proteins circulating in the blood)
Axillary
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

47. what cell surface marker is used for NK cells as it is unique to them?
CD56
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
A - B - C; all the D's
Cross link

48. Name 5 ways Antibody diversity is generated?
T cell precursor
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

49. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

50. other than C3a - what other complement acts as an anaphyloxin?
C5a
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)