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blood and lymph > Immunology > Flashcards

Immunology Flashcards

1
Q

Serum IgG

A

1000 mg/dL

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2
Q

Serum IgG

A

200 mg/dL

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3
Q

Serum IgM

A

100 mg/dL

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4
Q

Plasma 1/2 life of IgG

A

3 weeks

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5
Q

Proteins involved in complement Lytic function

A

MAC - C5 –> C6 C7 C8 C9 –> poke holes in membrane

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6
Q

Proteins involved in complement opsonizing function

A

C3b binds membranes
Phagocytotic cells (PMN, macrophages) have C3b receptors that give them a better grip
**IgG is also opsonizing (Phagocytotic cells have FcR) but IgM is not.

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7
Q

Proteins involved in complement chemotactic function

A

C5a is chemotactic or phagocytes (esp. neutrophils) This explains much of the inflammatory response seen in complement

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8
Q

Proteins involved in Anaphylotoxic function of complement

A

C3a, C4a, and C5a release histamine from mast cells and basophils, allowing increased blood flow to area and increased inflammatory response.

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9
Q

Th0

A

Undifferentiated Helper T cell precursor
All have CD4 and begin in paracortex of lymph node
When DC arrives w/correct antigen, they divide and differentiate (determined by DC determinants)

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10
Q

Th1

A

Circulate through body and secrete Lymphokines
IFNgamma*==> macrophage chemotaxis and M1 activation
IL-2==> CTL activation

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11
Q

M1/angry macrophage secretions

A

TNF alpha and IL-1

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12
Q

Th17

A

**Secretes Il-17
resistant to bacterial and yeast pathogens
activate M1

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13
Q

Chemokines

A

small, short range mediators that primarily cause inflammation

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14
Q

Th2

A

secrete* IL-4*, IL-5, IL-13 that attract and activate M2 macrophages!

IL-4 is also chemotactic for eosinophils

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15
Q

Tfh

A

Activated helper T’s migrate from paracortex to cortes and help B -cells to differentiate and class switch

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16
Q

Treg

A

T cells whose main job is to suppress activation of other Th Cells

  • Make Transcription factor Foxp3
  • Make TGF beta and IL-10
  • Respond to their antigen and suppress all nearby Th cells
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17
Q

CTL death signal

A

(1) engage Fas death receptor on target (CTL’s bear death ligand CD95L)
(2) Secrete ‘lytic granules’ which contain granzymes and perforins that lead to apoptosis

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18
Q

CTL activation

A
  • in lymph nodes, requrie Th1 and IL-2

* *need Il-21 to convert to memory cells**

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19
Q

Memory cells

A
  • sort of like immune stem cells

- self-replication, rapidly differentiate into helper and killer when re-exposed to antigen

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20
Q

T cell markers

A 
CD3- all T Cells
CD4 - all helpers
CD8 - CTL's
(these play a role in T cell activation)
CD20 - B Cells
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21
Q

MHC restriciton

A

CTL’s only see antigen presented to them on the surface of a genetically identical cell.
Antigen-presenting cell must come from individuals who share MHC alleles

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22
Q

Antigen presentation extrinsic pathway

A

Something infects locally, breakdown products are phagocytosed by DC and then presented on the cell surface with an MHC.

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23
Q

T cell Receptor

A
  • Sort of looks like an antibody, but just two chains (alpha and beta)
  • Constant and Variable region
  • VDJ Variable regions recombine like in B cells in the thymus
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24
Q

CD3

A

-Transduces signal from TCR when it binds MHC

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25
Q

3 ways Th cells are activated by a good APC

A

(1) TCR sees the TCR-pMHC cell
(2) Accessory molecular interactions that modify activation
(3) Cytokines from APC

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26
Q

MHC class 1

A

Presented on all cells

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27
Q

MHC Class II

A

On the surface of dendritic and macrophage-type cells, B Cells, etc. (Antigen presenting cells!)

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28
Q

Which MHC does an antigen associate with if it’s taken up by the DC extrinsic pathway?

A

MHC II

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29
Q

Which T cells recognize peptides on MHC II molecules?

A

TH1, Th17, Tfh, Treg, Th2

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30
Q

Intrinsic pathway

A

antigen is a protein sampled from within the cell itself, presents on MHC I

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31
Q

Which T cells recognize stuff in MHC I?

A

CTL’s!

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32
Q

Cross-presentation

A

DC’s are wonderful, and they let peptides from antigens leak over into the “intrinsic pathway” so it presents on MHC I and II

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33
Q

What does CD4 bind on Th’s

A

The base of MHC II (CD8 binds base of MHC I

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34
Q

causes of increased hydrostatic pressure

A
  • Heart failure
  • Fluid overload
  • Venous obstruction or compression
  • Arteriolar dilation
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35
Q

Causes of decreased oncotic pressure

A
  • Protein loss (kidney, GI)

- Low protein production

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36
Q

Causes of lymphatic obstruction

A

Inflammation, infection, neoplasm

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37
Q

Hyperemia

A

Active increase in blood flow due to arteriolar dilation

Causes red color (erythema)

38
Q

Congestion

A

Pathologic accumulation of blood due to impaired venous clearance

39
Q

Virchow Triad

A

Endothelial Damage, Abnormal blood flow (stasis or turbulence) and hypercoagulability (inherited or acquired (cancer)

40
Q

Common cause of arterial thrombosis

A

Endothelial injury and turbulent blood flow, often associated with atherosclerosis
Most common in cerebral, coronary, and femoral arteries

41
Q

Thrombus progression

A

Initial thrombus is attached to the wall and additional layers propagate and eventually become less stable and throw thromboemboli

42
Q

Embolus

A

A free floating, intravascular mass of a solid, liquid, or gas

43
Q

Venous embolism common target

A

Lungs

44
Q

Arterial emboli common targets

A

Legs and Brain

45
Q

Disseminated intravascular coagulation (DIC)

A

thrombosis and hemorrhage occur concurrently

Involves a systemic activation of thrombin

46
Q

White (anemic) infarcts

A

Arterial blockage, single blood supply, dense tissue

Heart, kidney, spleen

47
Q

Red infarcts

A

When blood flow is subsequently reestablished, allowing flow into the necrotic area - lungs, liver, intestine

48
Q

Shock

A

circulating blood volume is not adequate to perfuse body tissues

49
Q

Cardiogenic Shock

A

failure of heart to pump blood to tissues/ generate adequate blood pressure
coolness and pallor of their skin, tachycardia, and decreased urine output

50
Q

Hypovolemic Shock

A

Not enough volume, not enough blood gets back to the heart to do its job
coolness and pallor of their skin, tachycardia, and decreased urine output

51
Q

Septic shock

A

High levels of inflammatory mediators in the blood cause widespread vasodilation, vascular leakage, and venous blood pooling.

52
Q

HLA

A

the family of genes that are important for histocompatibility in humans
HLA-A, HLA-B, and HLA-D
*HLA-DR is most important for transplant

53
Q

MHC III

A

HLA Loci that encode components of the complement system and certain cytokines

54
Q

MHC loci gene expression

A

co-dominant
(You’ll have mom’s and dad’s expressed on the surface of each cell)
HLA-D (MHC II) will only be expressed on antigen presenting cells

55
Q

AIRE gene

A

causes thymus to express a large variety of extrathymic peptides, helping to prevent autoimmunity against, say, Liver peptides

56
Q

Minor Histocompatibility antigens

A

H-Y a gene coded on Y-chromosome, the protein pdt is presented by MHC I, but only on male cells! (So female bodies reject male skin grafts, but NOT vice versa)

57
Q

Hyperacute Rejection

A

A graft is given to a patient who has preexisting antibody against the tissue (from prior graph/transfusion or in a mismatch)
Complement causes vasospasms (via anaphylatoxins and histamine)
Avoid by testing for cytotoxic antibodies before transplanting.

58
Q

Is Class I or Class II MHC match more important?

A

Class II!
►(1) If the donor and
recipient are identical at Class I but different at Class II, Th1 will be activated; but no CTL will
be activated, because there is no Class I difference for them to see. The graft will still be rejected,
but since only Th1 and not CTL would be involved, rejection may be slower. ►(2) If the donor
and recipient are different at Class I but identical at Class II, there will be no Th1 activated, no
IL-2 will be generated, and so few CTL will be activated.

59
Q

Ankylosing spondylitis

A

Arthritic condition in which there is inflammation at insertion of tendons into bones
followed by eventual calcification
92% of those people are HLA-B27

60
Q

Neoplasia

A

Autonomous, progressive cell growth involving clonal cell population

61
Q

Cyclophosphamide

A

for breast: combine with doxyrubicin, methotrexate and 5-fluorouracil

  • Also for lymphomas, childhood tumors, solid tumors
  • Must be activated by metabolism to phosphoramide mustard
  • Active metabolite is inactivated by Aldehyde dehydrogenase
62
Q

Alkylating agent repair resistance mxns

A

GSH inactivates alkylating agents

DNA repair

63
Q

Alkylating toxicity

A 
Hematopoietic (dose-limiting)
Intestinal toxicity
Gonadal toxicity
Alopecia
Carcinogenesis (leukemia)
64
Q

Cisplatin

A
  • Nephrotoxic
  • Crosslinks DNA (CpG)
  • Testicular cancer! Also ovarian, head and neck, lung, bladder
65
Q

Resistance to platinum compounds

A
  • Increased efflux/decreased cellular uptake
  • GSH inactivation
  • Loss of Mismatch Repair (also activates apoptosis)
66
Q

Platinum toxicity

A

**Nephrotoxicity!* (hydration!)
Nausea, ototoxicity, neurotoxicity

Carboplatin: myelosupression/ platelet toxicity
Oxaliplatin - sensory neuropathy

67
Q

5-fluorouracil

A

-pyrimidine analog
-Activated by thymidine kinase to FdUMP
FdUMP inhibits thymidilate synthase, inhibitin DNA synthesis
Other metabolites enter DNA/RNA- DNA DAmage–> apoptosis

68
Q

5-FU resistance

A

Alterations in target enzyme (TS)

Increase in Levels of TS (Drug leads to inactivation of normal feedback mechanisms to regulate TS levels. )

69
Q

5-FU toxicity

A

What you’d expect:
Myelosupression, gastro toxicity, alopecia
+ Derm problems

70
Q

Topo I inhibitors

A

campothesins (topotecan, irinotecan), epipodophyllotoxins

71
Q

Topo II inhibitors

A

etoposide, anthracyclines, doxorubicin, daunorubicin

72
Q

Topo interacting agent resistance

A

Increased efflux, topo mutations

73
Q

Topo interacting agent toxicity

A

Myelosupression (all)
Cardiotoxicity (anthracyclins - improved by Fe chelation)
Secondary malignancy (esp. AML after ALL treatment)

74
Q

Vinca Alkaloids

A

Vinca alkaloids (vinblastine and vincristine)

  • Bind tubulin and cause MT depolymerization
  • Ped malignancies, hematopoietic tumors, and some solid tumors
75
Q

Vinca resistance

A

Increased drug efflux (MDR transporters)

Tubulin mutations

76
Q

Vinca toxicity

A

Neurotoxicity (nerve cell damage)

Myelosupression, neutropenia

77
Q

Taxanes

A

Docetaxel, paclitaxol
Bind inside of microtubules and prevent mitosis–> apoptosis
Ovarian and breast+ other solid tumors

78
Q

Taxane resistance

A

Increased Efflux (MDR)
Tubulin mutation
Inhibited apoptosis

79
Q

Taxane toxicity

A

Myelosupression (neutropenia)
Peripheral neuropathy
Alopecia

80
Q

Hormonal Agents that block receptor activity

A

Tamoxifen - blocks estrogen receptor

Bicalutamide and flutamide block androgen receptor

81
Q

Hormonal agents that block hormone synthesis

A 
Aromatase inhibitors (Letrozole) block synthesis of estrogen from androgens (major source in post-menopausal people)
GNRH analogue (Leuprolide) inhibit testostrone production
82
Q

Resistance to steroid receptor inhibitors

A
  • Alternative activation mechanisms

- Mutations in receptor (if it’s mutated to be activated by chemo, withdrawl can inhibit tumor growth)

83
Q

Hormonal toxicities

A
  • Hormone signalling side effects in women (hot flashes, decreased bone density)
  • Gynecomastia in men treated with flutamide/bicalutamide)
84
Q

Rituximab

A

Anti-CD20 treats B cell tumor

85
Q

Trastuzumab/Herceptin!

A

Anti-Her2 for breast cancer

86
Q

Bevacizumab/Avastin

A

Anti-VEGF colon cancer

87
Q

Antibody chemo function

A

-Inhibits target function (Ex. Avastin blocks VEGF from stimulating receptor to promote angiogenesis
Also, CTL response can occur in response to antibodies
Immunoconjugates can also deliver toxins, chemotherapueutic drugs, radioisotopes to tumor cells

88
Q

Kinase Inhibitors

A

Targeted
Best ex. Imatinib for CML and GIST
But MOST don’t cure cancer on their own and resistance to therapy almost always occurs

89
Q

CML

A

caused by BCR-abl constituitively active kinase, inhibited by imatinib

90
Q

Dasatinib

A

A drug that works in CML patients with mutated Bcr-Abl resistant to Imatinib

blood and lymph (2 decks)

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