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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. For which toxins are preformed antibodies (passive) given?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Para aortic
Lymphocytes
Tetanus - Botulinum - HBV - Rabies

2. Monomer in circulation - ___ when secreted
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
Macrophages - Dendritic cells - B cells
TNF alpha and IL1
dimer

3. describe the classic complement pathway.
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Barrel hoop basement membrane fenestrations
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

4. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

5. where do somatic hypermutation and class switching occur?
Anti smooth muscle
Para aortic
In the germinal center of secondary follicles (In the paler center)
Previous transfusion; pregnant woman whose fetus had paternal antigens

6. The Fc region is found on the...
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
carboxy terminal
IgM and IgA
active complement pathway

7. What are the autoantibodies for pernicious anemia?
Antidesmoglein
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Anti IF

8. Which disease is associated with B8?
Graves
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

9. what characterizes an arthus reaction?
Edema and necrosis in that region
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Remove encapsulated bacateria
Antibody mediated cytotoxicity; either complement dependent or complement independent

10. Which disease is associated with HLA A3?
Hemochromatosis
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Interferon gamma and IL 2
2 heavy chains and two light chains

11. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Anti smooth muscle
No because no peptide fragment!
...
Superficial inguinal

12. What lymph node drains the upper limb?
By transcytosis
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Axillary
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

13. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
T cell activation; no with CD 4 or CD 8
Its main effect is a defect in Ab opsonization for killing
Activate macrophages
Paracortex

14. when can graft versus host disease? What is the result?
CRP - C3b - IgM
Macrophages - Dendritic cells - B cells
CD56
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

15. How fast does it occur?
Cyclosporine - OKT3
Humoral
The patient could become cyanotic in the OR!
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

16. 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
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
Anti Ach receptor
Fc

17. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
T cell activation; no with CD 4 or CD 8
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

18. Type IV hypersensitivity is i...
Anti topoisomerase
T cell activation; no with CD 4 or CD 8
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
not Ab mediated

19. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
Macrophages - Dendritic cells - B cells
IgM and IgG
delayed!

20. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Anti glutamate carboxylase and anti insulin
TLR ad nuclear receptors
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

21. where do NK cells develop?
Not thymus - BM
Superior mesenteric
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
T cell dysfunction

22. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Immunosuppression after kidney transplantation

23. Which antibodies can be multimeric?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgM and IgA
Para aortic

24. where are complements produced?
Wiskott Aldrich syndrome
SP infections
Secretory component
Liver! (they are proteins circulating in the blood)

25. What are the autoantibodies for graves?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti TSh receptor
T cell dysfunction

26. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgG
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

27. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Axillary
Superior mesenteric

28. What are the autoantibodies for wegeners granulomatosis?
Immunoflourescent staining of tissue biopsies
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Negative nitroblue tetrazolium reduction test
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

29. What are the mediators that mast cells release?
Daclizumab; prevent ACUTE rejection of renal transplant
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IL 4

30. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Liver! (they are proteins circulating in the blood)
Cytokine IL 10 secreted by Th2
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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

31. What is the main cytokine that activates eosinophils?
Macrophages - Dendritic cells - B cells
IL 5
TNF alpha and IL1
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

32. What are the autoantibodies for drug induced lupus?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Antihistone
Celiac
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

33. other than C3a - what other complement acts as an anaphyloxin?
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
secondary
C5a

34. which antibody activate mast cells - basophils - and eosinophils?
IgE
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IL 1 and IL 6
Recom IL 11; thrombocytopenia

35. 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?
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
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
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
TLR ad nuclear receptors

36. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Paracortex
Cyclosporine - OKT3
Macrophages - Dendritic cells - B cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

37. what prevents NK cells from killing normal cells if their default is to kill?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
MHC class molecules bind to KIRS or CD94 to prevent killing
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
pathogenesis

38. What are the autoantibodies for myasthenia gravis?
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 4
Anti Ach receptor

39. What are the T cell functions?
Anti Jo -1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

40. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
heavy chains

41. 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?
Immunosuppression after kidney transplantation
Anti SS- A (anti RO) and Anti SS- B
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
If there is class switching and plasma cell production (that is when memory cells are produced)

42. How is i Th1 helper cell inhibited?
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
CRP - C3b - IgM
Cytokine IL 10 secreted by Th2
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

43. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Its a serine protease that activates apoptosis; NK and CD8
pathogenesis

44. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
The igA found in breast milk
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
DM type I
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

45. What type of fenestrations are found in the red pulp of the spleen?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
S. aureus - E. Coli - aspergillus
Barrel hoop basement membrane fenestrations
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

46. What are howell jolly bodies?
Rheumatic arthritis
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Pernicious Anemia and Hashimotos
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

47. What are the two signals required for Th1 cells? what happens after then activated?
acute phase reactants
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Sinusitis - otitis media - pneumonia

48. How do you test for chronic granulomatous disease?
Wiskott Aldrich syndrome
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Negative nitroblue tetrazolium reduction test

49. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Cross link
A j chain
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
IgM and IgG

50. 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 )
Anti Ach receptor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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

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USMLE Step 1 Immunology

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