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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 is hereditary angioedema? What are the C3 levels?
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
MS - hay fever - SLE - goodpastures
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

2. Monomer in circulation - ___ when secreted
dimer
IgE; by activating eosinophils
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

3. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Chronic granulomatous disease
isotype
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

4. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

5. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
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
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
Kill them because they have CD16 on them that recognize the FcG portion
Paracortex; viral infection

6. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
pathogenesis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Sinusitis - otitis media - pneumonia

7. Name two endogenous pyrogens
TLR ad nuclear receptors
IL 1 and IL 6
Viral neutralization of igM and IgG!
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

8. What does IgA pick up from epithelial cells before being secreted?
No because no peptide fragment!
Secretory component
lowest concentration
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

9. which interleukin receptor is required for NK development? activation?
Interferon gamma; Th1
IL 15; IL 12 - interferon Beta and interferon alpha
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Its a serine protease that activates apoptosis; NK and CD8

10. What happens in a secondary follicle?
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 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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

11. What are the three types of lymphocytes?
TNF alpha and IL1
...
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
B - T - and NK cells

12. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
...
Viral neutralization of igM and IgG!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

13. Which antibodies can be multimeric?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgM and IgA
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

14. What is the pathology of acute transplant rejection? is it reversible?
The patient could become cyanotic in the OR!
Secretory component
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

15. What are the two signals required for B cell class switching? Which is the second signal?
opsonizes
Chronic granulomatous disease
Its main effect is a defect in Ab opsonization for killing
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

16. What are the main symptoms of T cell immunodeficiencies?
IgM and IgA
active complement pathway
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Activates Th1 helper cells; Macrophages

17. Describe the Mannose Lectin pathway
carboxy terminal
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
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

18. in which immunodef order do you see a lot of pus? no pus?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

19. What are the function of B cells?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Alternative splicing of mRNA
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
The igA found in breast milk

20. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Wiskott Aldrich syndrome
Basophils! THey want IG E class switch!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Hereditary angioedema; PNH

21. what happens in a deficiency of C1 esterase inhibitor? DAF?
Anti U1 RNP (ribonucleoprotein)
Hereditary angioedema; PNH
Internal iliac
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

22. what characterizes an arthus reaction?
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
Anti alpha subunit 3 of collagen on type IV bm
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
Edema and necrosis in that region

23. What are the autoantibodies for polymyositis and dermatomyositis?
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
Anti Jo -1
T cell dysfunction
In the germinal center of secondary follicles (In the paler center)

24. which antibody activate mast cells - basophils - and eosinophils?
CRP - C3b - IgM
Anti TSh receptor
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
IgE

25. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Daclizumab; prevent ACUTE rejection of renal transplant
Antimicrosomal and antithyroglobulin
All MHC 1/CD8
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

26. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Hereditary angioedema; PNH
carboxy terminal
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

27. What are the two signals required for Th1 cells? what happens after then activated?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Anti mitochondrial
active complement pathway
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

28. What is the main function of TNF alpha? How does it do this?
Anti smooth muscle
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
neutrophilia!
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

29. What is recomb beta interferon used for?
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
MS
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

30. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IL 4
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

31. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti alpha subunit 3 of collagen on type IV bm
IL 5
Anti Ach receptor

32. What are the labs in brutons agammaglobulinemia?
DM type I and RA
Axillary
mesenchymal
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

33. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
pathogenesis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

34. What are the autoantibodies for Celiac disease?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Severe pyogenic infections early in life
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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

35. 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
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
Wiskott Aldrich syndrome
Antidote for digoxin intoxication

36. The pathogenesis of contact dermatitis is ________ hypersensitivity
Activate macrophages
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
type four
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

37. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
pentamer
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

38. What is the main cytokine that activates eosinophils?
IgM and IgA
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
IL 5
IL 15; IL 12 - interferon Beta and interferon alpha

39. What is muromonab - CD3 (OKT3)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Th cells fail to produce interferon gamma; a lot of IgE
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Glycoproteins; HLA

40. What portion of the lymph node is not well developed in DiGeorge Syndrome?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Paracortex
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

41. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
pentamer
Para aortic
All MHC 1/CD8

42. In thymic development - What is the positive selection? negative selections?
Internal iliac
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
When you select for which MHC it will have; take out the lymphs that self react
cannot cross placenta

43. What is the clinical use for sirolimus? what should you combine it with?
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
Celiac
Superficial inguinal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

44. IgG...
opsonizes
Hemochromatosis
not Ab mediated
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

45. Which diseases are associated with DR4?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
DM type I and RA
Chronic granulomatous disease
Paracortex; viral infection

46. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
heavy chains
Activate macrophages
Th2; Th1

47. How fast does it occur?
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 5
The patient could become cyanotic in the OR!
Anti SS- A (anti RO) and Anti SS- B

48. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti SS- A (anti RO) and Anti SS- B
Kill them because they have CD16 on them that recognize the FcG portion

49. 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
A - B - C; all the D's
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

50. What does granulysin do?
Secretory component
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Superior mesenteric
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata