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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 is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
NK cells
Anti glutamate carboxylase and anti insulin

2. What is the toxicity of muromonab?
dimer
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

3. What are the two signals required for T cells? what happens after?
IL 5
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Its main effect is a defect in Ab opsonization for killing
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

4. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
B - T - and NK cells

5. What kinds of receptors activate innate immunity?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
SP infections
Activate macrophages
TLR ad nuclear receptors

6. Which antibodies can be multimeric?
No because no peptide fragment!
Remove encapsulated bacateria
IgM and IgA
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

7. What lymph node drains the thigh?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Superficial inguinal
Negative selection
Previous transfusion; pregnant woman whose fetus had paternal antigens

8. What is passive immunity?
opsonizes
Antidote for digoxin intoxication
Receiving preformed Antibodies
Kill them because they have CD16 on them that recognize the FcG portion

9. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
TLR ad nuclear receptors
IL 15; IL 12 - interferon Beta and interferon alpha

10. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
T cell activation; no with CD 4 or CD 8
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

11. What is immune complex disease? give an example.
Bind FcG for antibody dependent cellular cytotoxicity
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

12. Which diseases are associated with DR4?
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
...
DM type I and RA
False! B cell class switching requires a second signal

13. 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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

14. Describe the complement independent Type II hypersenstivity reaction. Give an example.
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
In the germinal center of secondary follicles (In the paler center)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

15. The ______ in the BM are DN - the DP are in the cortex of thymus
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
T cell precursor

16. The alternative pathway is the only constutively...
lowest concentration
Superior mesenteric
active complement pathway
Fc

17. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
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
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
IgG

18. What happens in a secondary follicle?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
opsonizes
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

19. What is hereditary angioedema? What are the C3 levels?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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 mitochondrial
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

20. What is the pathology seen in chronic transplant rejection?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Celiac
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Yes

21. What are the autoantibodies for drug induced lupus?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Antihistone

22. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Severe pyogenic infections early in life
Anti topoisomerase
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

23. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
...
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

24. What are the autoantibodies for graves?
Anti TSh receptor
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Activate macrophages
not Ab mediated

25. where are complements produced?
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
Local infection/inflammation; infection of the ln itself; metastasis
Liver! (they are proteins circulating in the blood)
T cell activation; no with CD 4 or CD 8

26. What are the three types of lymphocytes?
B - T - and NK cells
Histamine; post capillary venules - vasodilation
except hyperacute
A chemotactic factor for neutrophils

27. What bugs can actually infect the lymph node itself?
Anti SS- A (anti RO) and Anti SS- B
Antidote for digoxin intoxication
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

28. What portion of the lymph node is not well developed in DiGeorge Syndrome?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Paracortex
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
Sinusitis - otitis media - pneumonia

29. What are the main Cell surface proteins on T cells?
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
Kill them because they have CD16 on them that recognize the FcG portion
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
The igA found in breast milk

30. what mediates the type II hypersensitivity? What are the two different methods?
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
MHC class molecules bind to KIRS or CD94 to prevent killing

31. The Fc region is found on the...
carboxy terminal
Sinusitis - otitis media - pneumonia
IL 1 and IL 6
isotype

32. What is the main cytokine that activates eosinophils?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgM and IgD
IL 5
IL 4 - 5 - 10 - 6

33. What is the most common example of passive immunity?
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 :(
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgAs in mothers breast milk!
Antihistone

34. What is a type I hypersensitivity reaction? What is atopic?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Lymphocytes
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Internal iliac

35. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Antidesmoglein
T cell activation; no with CD 4 or CD 8
TLR ad nuclear receptors

36. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

37. What are the autoantibodies for pemphigus bulgaris?
lowest concentration
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
Histamine; post capillary venules - vasodilation
Antidesmoglein

38. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
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 I - CD16 - CD56
...
pathogenesis

39. How does complement link innate and adaptive?
C5a
TNF alpha and IL1
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti U1 RNP (ribonucleoprotein)

40. What is the toxicity of azathioprine?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgG
...
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

41. What is an example of a parasite showing antigenic variation?
Carbohydrate
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Complement activation (active in both)

42. What lymph node drains the testes?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Its main effect is a defect in Ab opsonization for killing
type four
Para aortic

43. What is the main function of TNF alpha? How does it do this?
Cyclosporine - OKT3
heavy chains
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

44. How does igA cross the epithelium?
Axillary
Increases expression of MHC I and MHC II and also activates NK cells
TLR ad nuclear receptors
By transcytosis

45. What does granzyme do? who secretes it?
delayed!
When you select for which MHC it will have; take out the lymphs that self react
Its a serine protease that activates apoptosis; NK and CD8
CD56

46. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
except hyperacute
A - B - C; all the D's
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

47. Which disease is associated with HLA A3?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Hemochromatosis

48. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MS
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

49. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgM
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

50. What is the pathogenesis of acute transplant rejection? When does it occur?
Remove encapsulated bacateria
Negative nitroblue tetrazolium reduction test
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Anti U1 RNP (ribonucleoprotein)