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IHO > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What is the “other” name for factor 2?

A

thrombin

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2
Q

What factors are in the intrinsic pathway?

A

-Factors VIII, IX, X, XI, and XII; factor VIIIa is a cofactor

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3
Q

What factors are in the extrinsic pathway?

A

Tissue factor (TF) and Factor VII

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4
Q

Which factors require vitamin K-dependent gamma carboxylation?

A

Factors II, VII, IX, X, Proteins C and S

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5
Q

Why does Warfarin (Coumadin) when started need to be “bridged” with heparin?

A

-since Warfarin blocks proteins S and C it can caused increased clotting before it starts working correctly

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6
Q

Anti-thrombin 3 interacts with which drug?

A

Heparin

-ATIII leads to thrombin inactivation; also blocks the activity of factors VIIIa, IXa, Xa, and XIa

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7
Q

Why is aspirin an irreversible platelet inhibitor?

A

-blocks COX 1 (platelets don’t have nuclei so can’t make more)

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8
Q

How does activated protein S affect the coagulation cascade?

A

-degrades factors Va and VIIIa via proteolysis thereby decreasing thrombin production

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9
Q

GP 1b deficiency causes what syndrome?

A

Bernard Soulier syndrome

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10
Q

What CD is the IL-2 receptor?

A

CD25

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11
Q

What marker targets APCs to the lymph nodes?

A

CCR7 (in lymph nodes activates T cells)

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12
Q

What signals does an immunogenic DC produce to activate T cell proliferation and pro-inflammatory cytokines?

A

CD86hi, MHC2 hi, CD40 hi, CCR7 hi

-pro-inflammatory cytokines = IL-12 and TNF-alpha

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13
Q

What signals do tolerogenic DCs produce to stimulate clonal deletion or anergy of antigen-specific T cells?

A

CD86 lo, MHC 2 lo, CD40 lo, CCR7 lo

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14
Q

what are the 4 types of Treg mechanisms to control proliferation/ actions of other T cell populations?

A
  1. immunosuppressive cytokines (IL-10, TGF-beta, IL-35)
  2. IL-2 consumption
  3. cytolysis (granzyme mediated)
  4. modulation of DC maturation and function (kynurenin causes cell cycle arrest and CD 152/ CTLA4)
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15
Q

What are the 4 main mechanisms of B cell tolerance?

A
  1. clonal deletion (inhibition of survival signals or activation death receptors)
  2. receptor editing (continued V(D)J recombination)
  3. B-cell intrinsic mechanisms (anergy, down-regulation of BCR, upregulation CD5)
  4. lack of T-cell help or survival factors
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16
Q

What cytokines do Th1 cells produce?

A

-IFN-gamma, TNF-beta, IL-2

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17
Q

What cytokines do Th2 cells produce?

A

-IL-4, IL-5, IL-9, IL-10, IL-13

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18
Q

What cytokine does Th17 produce?

A

IL-17A (neutrophil recruitment/ inflammation)

-TNF-alpha

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19
Q

What are the 2 mechanisms for antibody-dependent B cell suppression?

A
  1. IgG can cross-link Ag receptor with Fc receptor on same cell
  2. IgM and IgG can act to modulate immune response through Fc-dependent mechanism and immune complex formation with antigens
20
Q

What is the 1 mechanism of antibody-dependent B cell augmentation?

A

by activating complement, immune complexes may become localized via interactions with CR2 on follicular dendritic cells (facilitates immune response by maintaining source of Ag)

21
Q

What gene is mutated in IPEX?

A
  • lack of both CD4+/CD25+ cells and CD4+ Foxp3 positive cells
  • mutation in FOXP3 gene (make Treg cells)
22
Q

What are the key features of IPEX? Physical manifestations?

A
  • autoimmune problems

- intractable watery diarrhea, FTT, dermatitis, autoimmune diabetes in infancy

23
Q

What abnormalities present in a WBC differential for IPEX?

A
  • normal WBC count, normal HgB, normal platelet count

- elevated percentage eosinophils and elevated IgE

24
Q

Treatment for IPEX?

A
  • immunosuppressive therapy

- bone marrow transplant

25
Q

What does Coumadin block?

A

Vitamin K

26
Q

What receptor do Abciximab, Eptifibatide, and Tirofiban block?

A

GPIIb-IIIa receptor

-inhibits final common pathway for platelet aggregation

27
Q

Which enantiomer of Warfarin is more active?

A

-S enantiomer

28
Q

What do Ticlopidine, Clopidrogrel, Prasugrel, Cangrelor, and Ticagrelor block?

A

ADP recruiting and activating platelets

29
Q

What is the difference between direct and indirect agglutination?

A
  • Direct: use Ab to bind surface of whole cell particle and watch for response (visualize after Fab portion of antibody has bound Ag)
  • Indirect: Ab has been mixed with something it can bind to so we can see agglutination (not directly binding) (visualize because Tc portion of Ab was bound to colored latex bead so when Fab portion binds to antigen the beads clump together)
30
Q

Direct ELISA: what starts out on plate? detect what? how detect? what gets washed away?

A
  • Abs to virus bound to plate
  • add Ag then 2nd antibody; wash unbound 2nd Abs
  • amount of colored product produced is proportional to amount of Ag
31
Q

Indirect ELISA: what starts out on plate? detect what? how detect? what gets washed away?

A
  • antigen on plate
  • add patient serum; wash
  • add anti-IgG conjugate to enzyme; wash
  • add substrate
  • Amount colored product is proportional to Ab concentration
32
Q

What are the different interpretations of being able to detect IgM or IgG antibodies in patient sera?

A
  • IgM: single, acute; positive= primary or current infection
  • IgG: acute= positive (4x rise or fall), negative= no current or past infection
  • IgG: single specimen= adult positive (infection at some time); newborn positive (got Abs from mom)
33
Q

Competitive ELISA: what starts out on plate? detect what? how detect? what gets washed away?

A
  • mix patient specimen with antigen with known amount of Ag-specific Ab
  • add specimen to Ag- coated plate
  • add anti-IgG conjugated to enzyme
  • add substrate
  • Colored product is inversely proportional to Ag concentration in patient serum
34
Q

What is hemagglutination used for?

A

-detection of viruses and of antiviral antibodies

35
Q

What are the 3 components of the HAT media? functions?

A

-Hypoxanthine (GTP precursor)
-Amino pterin (blocks TTP and GTP synthesis; blocks DHFR enzyme)
-thymidine
Goal is to only have fusion hybridoma cells survive (not myelnoma cells)

36
Q

Details behind the 3 hemagglutination assays?

A

1) detect Abs against RBCs
2) detect viruses that can agglutinate RBCs
3) detect Abs against viruses that can agglutinate RBCs
- hemagglutination inhibition rxns used for detecting viruses and anti-viral Abs

37
Q

How do you perform a hemagglutination inhibition reaction?

A

-perform a serial dilution of patient’s antiserum in a micro-titer plat; then add relevant virus and RBCs to each well; if patient’s antiserum has anti-HA Abs that bind the influenza strain being tested the Abs attach to the HA molecules and prevent hemagglutination

38
Q

What type of Ig is the most common in myeloma?

A

IgG= 60%; IgA= 20%; IgE and IgD are rare; never IgM

“Georgia Educational = GA Ed”

39
Q

Which Ig is elevated in Waldenstrom macroglobulinemia?

A

IgM (commonly also affects vision)

-presentation sounds like myeloma but can’t be with IgM

40
Q

What is the classic triad of myeloma?

A

anemia, bone pain, renal failure

41
Q

Which GP binds collagen? Which binds vWF? Which binds fibrinogen?

A
  • GP1a- collagen
  • GP1b- vWF
  • GP2b-3a- fibrinogen
42
Q

What does vWF do?

A
  • glues platelets to endothelium

- carries factor VIII

43
Q

What hereditary bleeding disorder is caused from lack of IIb-IIIa?

A

Glanzmann Thrombasthenia

-no aggregation; severe bleeding (receptor IIb-IIIa usually binds fibrinogen)

44
Q

What are the anticoagulant, fibrinolytic, and anti-inflammatory properties of Protein C?

A
  • anticoagulant: inactivates Va and VIIIa
  • fibrinolytic: promotes t-PA action
  • anti-inflammatory: keeps cytokines low
45
Q

What are the effects of antiphospholipid antibodies in vivo? in vitro?

A
  • in vivo: promote coagulation

- in vitro: inhibit coagulation (cause prolonged PTT/PT tests)

IHO (7 decks)

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