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Immunology Flashcards

1
Q

X-linked (Bruton) agammaglobulinemia

A

Defect in BTK, a tyrosine kinase gene which results in no B cell maturation. XR. Common in Boys. Recurrent bacterial and enteroviral infections after 6 months old. **dec Ig of all classes, absent/scant lymph nodes. **Normal CD19+ B cell count, dec pro-B.

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2
Q

Selective IgA deficiency

A

Most common 1° immunodeficiency. Asymptomatic, can see Airway and GI infections, Autoimmune disease, Atopy, Anaphylaxis to IgA-containing products. IgA<7mg/dL with normal IgG and IgM levels

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3
Q

Common variable immunodeficiency

A

defect in B-cell differentiation. Acquired in 20-30s, inc risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infection. Dec plasma cells and immunoglobulins

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4
Q

Thymic aplasia (DiGeorge Syndrome)

A

22q11 deletion; failure to develop 3rd and 4th pharyngeal pouch, absent thymus and parathyroids. Tetany (hypocalcemia), recurrent viral/fungal infections (T cell deficiency), conotruncal abnormalities (tetrology of fallot, truncus arteriosus). Dec T cells, dec PTH, dec Ca2+. **Absent thymic shadow on CXR, FISH detection of 22q11 deletion. **

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5
Q

IL-12 receptor deficiency

A

dec TH1 response. AR. Disseminated mycobacterial and fungal infections; may present after administration of BCG vaccine. decreased IFN-y (secreted by TH1 cells)

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6
Q

Autosomal dominant hyper-IgE syndrome (Job syndrome)

A

deficiency of TH17 cells due to STAT3 mutations so impaired recruitment of neutrophils to sites of infection. FATED: coarse Facies, cold (noninflamed) staphylococcal Abscesses, retained primary Teeth, inc IgE, Dermatologic problems (eczema). inc IgE and dec IFN-y

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7
Q

What is the role of IFN-y?

A

Secreted from TH1 cells and activates macrophages. Important in granuloma formation and maintainene.

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8
Q

Severe combined immunodeficiency (SCID)

A

defective IL-2R gamma chain or adenosine **deaminase deficiency. **Filaure to thrive, chronic diarrhea, thrush. Recurrent viral, bacterial, fungal, and protozoal infections. Dec T cell receptor excision circles (TRECs). Absense of thymic shadow, germinal centers and T cells on flow cyto,etru. Tx: bone marrow transplant (no concern for rejection, yippee)

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9
Q

Wiskott-Adlrich syndrome

A

mutation in WAS gene, T cells unable to reorganize actin cytoskeleton. WATER: Wiskott-Aldrich, Thrombocytopenic purpura, Eczema, Recurrent infection. Increased risk of autimmune diseas and malignancy. inc IgE and IgA, low/normal IgG and IgM

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10
Q

Chronic Granulomatous Disease

A

defective NADPH oxidase, dec ROS. Suseptible to PLACESS: Pseudomonas, Listeria, Aspergillus, Candida, E.coli, Serratia, Staph aureus (nocardia, burkholderia cepacia)

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11
Q

What drains to the para-aortic lymph nodes?

A

testes, ovaries, kidneys and uterus

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12
Q

What drains to the internal iliac lymph nodes?

A

lower rectum to anal canal (above pectinate line), bladder, vagina and prostate

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13
Q

What drains to the popliteal lymph nodes?

A

dorsolateral foot, posterior calf

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14
Q

What drains to the axillary nodes?

A

upper limb, breast, and skin above the umbilicus

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15
Q

What enters the right lymphatic duct?

A

drains right side of body above the diaphragm

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16
Q

What does the thoracic duct drain?

A

everything that the right lymphatic duct doesn’t get, and enters in the left subclavian and internal jugular veins.

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17
Q

Why are asplenic patients at higher risk for encapsulated bacterial infections?

A

No spleen means less IgM production and decreased complement activation therefore less C3b opsonization of encapsulated bacteria

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18
Q

What are the encapsulated bacteria that asplenic patients are suspetible to?

A

SHiNE SKiS (or Even Some Pretty Nasty Killers Have Shiny Bodies):

Streptococcus pneumoniae

H. influ

N. meningitidis

E. coli

Salmonella

Klebsiella pneumoniae

Group B Strep

Klebsiella

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19
Q

Which bacteria from that infect asplenic patients have vaccines?

A

S. pneumo, H. flu type B, and N. meningitidis

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20
Q

What pharyngeal pouch is the thymus from?

A

3rd pharyngeal pouch!

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21
Q

HLA-A3 association?

A

Hemochromatosis

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22
Q

HLA-B27 assocations?

A

PAIR.

Psoriatic arthritis

Ankylosing spondulitis

IBD arthritis

Reactive arthritis

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23
Q

HLA-DQ2/DQ8 associations?

A

celiac disease

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24
Q

HLA-DR2 assocations?

A

MS, hay fever, SLE, Goodpasture syndrome

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25
Q

HLA-DR3 associations?

A

DM1, SLE, Graves disease

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26
Q

HLA-DR4 assocations?

A

Rheumatoid arthritis, DM1 (4 walls in a rheum)

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27
Q

HLA-DR5 associations?

A

pernicious anemia leads to B12 deficiency, hasimoto thyroiditis

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28
Q

What is the role of TNF-alpha in granuloma formation?

A

Secreted from macrophages and maintains the granuloma. If on anti-TNF therapy then need to first make sure they don’t have TB, or else it will become reactivated and disseminated.

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29
Q

What receptor recognizes LPS of gram - bacteria?

A

CD14 (TLR4) on macrophages

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30
Q

What results from TLR activation via recognition of a PAMP?

A

upregulation os NF-KB whihch is a nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators

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31
Q

What 4 key mediators activate neutrophils?

A
  1. LTB4
  2. C5a
  3. IL-8
  4. bacterial products
32
Q

Action of PGI2, LTD4, and PGE2?

A

mediate vasodilation @ arteriole and increased vascular permeaility @ post-capillary venule

33
Q

Action of LTC4, LTD4, and LTE4?

A

vasoconstriction, bronchospasm and increased vascular permeability

34
Q

How are mast cells activate?

A
  1. tissue trauma, 2. complement C3a and C5a, and 3. cross-linking of cell-surface IgE by antigen
35
Q

Main action of luekotrienes?

A

part of the delayed response to inflammtion and mainstains the acute infalmmatory response

36
Q

How is the classicla pathway activated?

A

C1 binds IgG or IgM (GM makes classic cars)

37
Q

What components make up MAC?

A

C5b-C9

38
Q

Describe the kinin system?

A

Activated by Factor XII, and then Kinin cleaves high-molecular weight kinogen to bradykinin which is a vasodilator and increases vascular permiability and causes pain.

39
Q

What enzymes lead to production of prostaglandins?

A

cycloxygenase

40
Q

What enzyme leads to production of leukotrienes?

A

5-lipoxygenase

41
Q

etiology of a fever?

A

pyrogens (LPS) cause macrophages to release IL-1 and TNF which increases COX activity so increased PGE2 production which raises the temp set point.

42
Q

Factors involved in margination?

A

vasodilation resulting in slower blood flow allowing neutrophils to flow on the periphery

43
Q

Factors involved in Rolling of neutrophils?

A

P-selectin released from Weibel-Palade bodies in endothelial cells and E-selectin induced by TNF and IL1. These selectins bind sialyly Lewis X on neutrophils

44
Q

Factors invovled in firm adhesion of neutrophils?

A

ICAM and VCAM on endothelial cells by TNF and IL1. Intigrins are upregulared on leukocytes by C5a and LTB4

45
Q

Factors invovled in transmigration and chemotaxis?

A

migrate across postcapillary venules and more toward injury via IL-8, C5a, LTB4and bacterial products

46
Q

How do you differnetiate between CGD caused by NADPH oxidase deficiency or MPO deficiency?

A

NADPH oxidase = negative Nitroblue tetraolium test

MPO= positive NBT test (turns blue)

47
Q

MPO deficiency puts you at an increased risk for what infections?

A

Candida

48
Q

What is the time frame in acute inflammation for Neutrophils and macrophages?

A

Neutrophils appear in the first 24 hours then disapear. Macrohpages predominatne 2-3 days after initiation of inflammation

49
Q

If you see pus, what type of inflammation is occuring?

A

acute inflammation

50
Q

Do macrophages predominantly use O2 dependent or independent killing?

A

O2-independent killing (lysozyme)

51
Q

What are the main cell types of acute inflammation vs. chronic inflammation?

A

acute = neutrophils and macrophages (innate immunity)

chronic = lymphocytes and plasma cells (adaptive immunity)

52
Q

How are CD4 helper cells activated?

A

MHCII on APCs presents the antigen to CD4 cells and then B7 on APC interacts with CD28 on CD4 helper cells.

53
Q

What do TH1 cells secrete?

A

IFN-y (activated macrophages, promotes B cell class-switching to IgE), IL-2

54
Q

What do TH2 cells secrete?

A

IL-4 (B-cells make switch to make IgE), IL-5, IL-6, IL-13 (similar function to IL-4)

55
Q

What provides the second signal in TH1 cell activation?

A

IL-2

56
Q

What is the role of caspase?

A

pathway involved in apoptosis that is activated by CD8 T cells.

57
Q

CD40 and CD40L

A

CD40 receptor is on B cells and bind CD40L, involved in activation of B cells and inducing class-switching

58
Q

What are epitheliod histiocytes?

A

macrophages with abundant pink cytoplasm that are the defining cells of a granuloma

59
Q

Noncaseating Granulomatous inflammation characteristics?

A

NO CENTRAL NECROSIS, usually due to sarcoidosis, beryllium expsures, Crohn disease, and cat scatch disease

60
Q

Caseating Granulomatous inflammatory characteristics?

A

central necrosis and is characteristic of tuberculosis and fungal infections.

61
Q

Steps in granuloma formation? (for both caseating and non-caseating)

A
  1. macrophages present antigen to TH1 cells
  2. macrophages secrete IL-12 which induces CD4 helper T cells to differentiate into TH1 cells.
  3. TH1 cells secrete IFN-y which converts macrophages to epitheliod histiocytes and giant cells
62
Q

What are patients with SCID suseptible to?

A

fungal, viral, bacterial, and protozola infections

63
Q

What typeos of vaccines must be avoided in Brutons Agammaglobulinemia?

A

live vaccines (polio)

64
Q

C1 esterase inhibitor deficiency?

A

results in hereditary angioedema, which is characterized by edema of the skin, **especially periorbital. **Increases bradykinin (ACEi contraindicated)

65
Q

What are the permanent tissues?

A

myocardium, skeletal muscle, and neurons. Lack significant regenerative potential

66
Q

What are the labile tissues?

A

tissues that posess stem cells that continuously cycle to regnerate capacity of tissue. stem cells in mucosal crypts, basal layer of skin, and hematopoietic stem cells in bone marrow

67
Q

What are the stable tissues?

A

Tissues made of cells that are quiescent (G0) but can reenter the cell cycle when necessary. **Liver **and kidney

68
Q

What is collagenase?

A

removes type III collagen from granulation tissue and uses zinc as a cofactor.

69
Q

What type of collagen is a hypertrophic scar made of?

A

type I collagen

70
Q

What type of collagen is a keloid made of?

A

type iII collagen

71
Q

where does hydroxylation of proline and lysine procollagen occur and what is the cofactor?

A

Occurs in the RER and vitamin C is the cofactor

72
Q

Where does cross-linking of collagen occur and what is the necessary cofactor?

A

occurs extracellularly and copper is the cofactor for lysyl oxidase which performs the cross-linking between lysine and hydrozylysine. Deficiey in this process = ehlers-danlos

73
Q

C3 deficiency?

A

increased risk of severe, recurrent pyogenic sinus an (S. pneumo and H. flu), increased susceptibility to type II hypersensitivity reactions

74
Q

What are the acute phase cytokines?

A

IL-1, IL-6 and TNF-alpha

75
Q

Function of TNF-alpha?

A

mediates septic shock, activates endothelium, leukocyte recruitment, maintains granulomas.

76
Q

What are the common passive antibodies that are given to patients?

A

To Be Healed Rapidly

Tetanus toxin

Botulinum toxin

HBV

Rabies

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