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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 pathology in hyperacute transplant rejection?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Th2; Th1
Receiving preformed Antibodies

2. What are the autoantibodies for drug induced lupus?
dimer
Humoral
When you select for which MHC it will have; take out the lymphs that self react
Antihistone

3. Which HLA's are included in MHC I? MHC II?

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4. What lymph node drains the testes?
Chronic granulomatous disease
Pernicious Anemia and Hashimotos
Macrophages - Dendritic cells - B cells
Para aortic

5. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
A chemotactic factor for neutrophils
IgG

6. What happens in a secondary follicle?
active complement pathway
Alternative splicing of mRNA
except hyperacute
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

7. Which disease is associated with B8?
Edema and necrosis in that region
Popliteal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Graves

8. What are the autoantibodies for pernicious anemia?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Humoral
Anti IF
Delayed type hypersensitivity

9. 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 )
2 heavy chains and two light chains
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
pathogenesis

10. What does interferon gamma do to be antiviral?
Secretory component
Increases expression of MHC I and MHC II and also activates NK cells
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

11. What are the autoantibodies for hashimotos?
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
Anti IF
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Antimicrosomal and antithyroglobulin

12. Describe complement dependent Type II hypersensitivity. Give an example.
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Cyclosporine - OKT3
pale central germinal centers

13. 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
Anti glutamate carboxylase and anti insulin
Immunosuppression after kidney transplantation
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

14. What is oprelevkin? and What is it used for?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
T
Recom IL 11; thrombocytopenia

15. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Antidesmoglein
A - B - C; all the D's
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

16. What lymph node drains the breast?
Th2; Th1
Axillary
neutrophilia!
IgA

17. How do you test for type III hypersensitivity?
carboxy terminal
Immunoflourescent staining of tissue biopsies
Severe pyogenic infections early in life
Interferon gamma and IL 2

18. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Antimicrosomal and antithyroglobulin

19. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Anti Ach receptor
Graves
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

20. What is immune complex disease? give an example.
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
MS
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IL 5

21. How is the thymus organized? what happens in each section?
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Superficial inguinal

22. What is three common causes of severe combined immunodef? What is the result of all three?
except hyperacute
Basophils! THey want IG E class switch!
MS - hay fever - SLE - goodpastures
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

23. Which disease is associated with DR7?
Rheumatic arthritis
Steroid responsive nephrotic syndrome
All MHC 1/CD8
Edema and necrosis in that region

24. which type of immunity is slow but long lasting? as opposed to...
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Active; passive - fast but short half life (3 weeks!)
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
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

25. What are the three types of APCs?
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
Macrophages - Dendritic cells - B cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
dimer

26. What is filgrastim and sargramostim? and What is it used for?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Stimulate the liver to release acute phase reactants
IL 4 - 5 - 10 - 6

27. What are the main cell surface proteins on B cells?
In the germinal center of secondary follicles (In the paler center)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

28. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

29. What is the presentation of scid? treatment?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

30. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Cross link
DM type I and RA

31. What lymph node drains the scrotum?
Superficial inguinal
Celiac
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

32. Monomer in circulation - ___ when secreted
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
dimer
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

33. Which is the main antibody in the delayed or secondary response to an antigen?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Sinusitis - otitis media - pneumonia
Fab portion
IgG

34. Leukocyte adhesion defect presents with...
neutrophilia!
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Local infection/inflammation; infection of the ln itself; metastasis
Negative nitroblue tetrazolium reduction test

35. What is chronic mucocutaneous candidiasis d/t?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Liver! (they are proteins circulating in the blood)
T cell dysfunction

36. 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?
IgM and IgG
Anti TSh receptor
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
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

37. what mediates the type II hypersensitivity? What are the two different methods?
Carbohydrate
Antibody mediated cytotoxicity; either complement dependent or complement independent
IgE; by activating eosinophils
IgE

38. What is epo used for?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anemias (esp due to renal failure)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

39. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Recom IL 11; thrombocytopenia
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

40. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
...
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
Increases expression of MHC I and MHC II and also activates NK cells

41. The two heavy chains of an antibody contribute to the...
All MHC 1/CD8
Fab portion
cannot cross placenta
IgAs in mothers breast milk!

42. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Rheumatic arthritis
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

43. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
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
Celiac
Barrel hoop basement membrane fenestrations

44. What is hereditary angioedema? What are the C3 levels?
Immunoflourescent staining of tissue biopsies
Local infection/inflammation; infection of the ln itself; metastasis
Wiskott Aldrich syndrome
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

45. Name 5 ways Antibody diversity is generated?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Anti IF
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

46. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti alpha subunit 3 of collagen on type IV bm
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

47. What is the common variable immunodeficiency ? How is it different from Brutons?
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
A - B - C; all the D's
Bind FcG for antibody dependent cellular cytotoxicity
If there is class switching and plasma cell production (that is when memory cells are produced)

48. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Negative selection
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Yes

49. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Liver! (they are proteins circulating in the blood)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Macrophages - Dendritic cells - B cells

50. Type IV hypersensitivity is i...
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
not Ab mediated
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Steroid responsive nephrotic syndrome