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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)?
Internal iliac
MHC I - CD16 - CD56
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti glutamate carboxylase and anti insulin

2. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
Anti smooth muscle
IgE

3. What are the autoantibodies for systemic sclerosis?
Anti SS- A (anti RO) and Anti SS- B
Negative!
Fc
Anti topoisomerase

4. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Superficial inguinal
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

5. What are target cells?
Basophils! THey want IG E class switch!
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
except hyperacute

6. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
IgA
Anti Ach receptor
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Paracortex; viral infection

7. What does Interferon alpha and beta do? how?
Not thymus - BM
Immunoflourescent staining of tissue biopsies
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Edema and necrosis in that region

8. What is the main function of interferons?
Anti alpha subunit 3 of collagen on type IV bm
Superior mesenteric
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Increases expression of MHC I and MHC II and also activates NK cells

9. Name the three opsonins
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
CRP - C3b - IgM
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
pale central germinal centers

10. The alternative pathway is the only constutively...
active complement pathway
S. aureus - E. Coli - aspergillus
neutrophilia!
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

11. What lymph node drains the upper limb?
Immunoflourescent staining of tissue biopsies
Axillary
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

12. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
MS
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
active complement pathway

13. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Pernicious Anemia and Hashimotos
Receiving preformed Antibodies
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

14. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anemias (esp due to renal failure)
Secretory component
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

15. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
In the germinal center of secondary follicles (In the paler center)
Celiac
IgE

16. Which disease is associated with DR7?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Superior mesenteric
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Steroid responsive nephrotic syndrome

17. What is three common causes of severe combined immunodef? What is the result of all three?
Activates cytotoxic CD 8 T cells as second signal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Influenza; antigenic shift; antigenic drift
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

18. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Daclizumab; prevent ACUTE rejection of renal transplant
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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 are the autoantibodies for goodpastures 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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti alpha subunit 3 of collagen on type IV bm
Its a serine protease that activates apoptosis; NK and CD8

20. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Superficial inguinal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Influenza; antigenic shift; antigenic drift
Antidote for digoxin intoxication

21. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Thrombocytopenia
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

22. What can cause a lymph node enlargement?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
secondary
Acts as second signal on B cells to induce class switching to IgE and IgG
Local infection/inflammation; infection of the ln itself; metastasis

23. 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)?
A recomb cytokine of IL 2; RCC and metastatic melanoma
T cell activation; no with CD 4 or CD 8
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
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

24. What is passive immunity?
Anemias (esp due to renal failure)
Wiskott Aldrich syndrome
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Receiving preformed Antibodies

25. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Lymphocytes
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

26. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IL 5

27. which of the hypersensitivity reactions is not Ab mediated?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Type IV
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
secondary

28. what cell surface marker is used for NK cells as it is unique to them?
Activate macrophages
CD56
Chronic granulomatous disease
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

29. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
IL 3; supports growth and differentiation of bone marrow stem cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cells that stil have weird parts of their membrane that macrophages usually bite off

30. The lymphocytes are ________ origin
mesenchymal
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
NK cells
Negative!

31. What is the clinical use for sirolimus? what should you combine it with?
Anti mitochondrial
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Barrel hoop basement membrane fenestrations
dimer

32. which interleukin receptor is required for NK development? activation?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IL 15; IL 12 - interferon Beta and interferon alpha
CD56

33. What cytokines to Th2 secrete?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
pale central germinal centers
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IL 4 - 5 - 10 - 6

34. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Celiac
secondary
Interferon gamma; Th1

35. What is the most common selective Ig deficiency? What is the presentation?
MHC II - B7
Its main effect is a defect in Ab opsonization for killing
Superficial inguinal
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

36. What does IL 5 do?
Hemochromatosis
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Anemias (esp due to renal failure)
Sinusitis - otitis media - pneumonia

37. T/F B cells do not require a second signal
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Chronic granulomatous disease
False! B cell class switching requires a second signal
IgG

38. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
T cell precursor
Delayed type hypersensitivity

39. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
delayed!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

40. What are the two signals required for Th1 cells? what happens after then activated?
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
carboxy terminal
Alternative splicing of mRNA

41. ________ regulate the cell mediated response.
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Humoral
Anti mitochondrial
Kill them because they have CD16 on them that recognize the FcG portion

42. what cytokine does basophils secrete?
A - B - C; all the D's
IL 4
Basophils! THey want IG E class switch!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

43. What is muromonab - CD3 (OKT3)
Sinusitis - otitis media - pneumonia
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 15; IL 12 - interferon Beta and interferon alpha
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

44. Only the _______ contribute to the Fc region
Thrombocytopenia
MHC I; from RER with help of the B2 microglobulin
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
heavy chains

45. For which toxins are preformed antibodies (passive) given?
Hereditary angioedema; PNH
Increases expression of MHC I and MHC II and also activates NK cells
T cell precursor
Tetanus - Botulinum - HBV - Rabies

46. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
If there is class switching and plasma cell production (that is when memory cells are produced)
Paracortex
Interferon gamma and IL 2

47. other than eat and bite RBCs what else do Macrophages of spleen do>
Edema and necrosis in that region
Antihistone
Anti glutamate carboxylase and anti insulin
Remove encapsulated bacateria

48. What are the three types of lymphocytes?
IL 1 and IL 6
...
B - T - and NK cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

49. What is the treatment of acute transplant rejection?
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
Cyclosporine - OKT3
Edema and necrosis in that region
Activates cytotoxic CD 8 T cells as second signal

50. In general What are T cells good for?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti viral and anti tumor
C5a
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)