Perf Tech Test 10 Flashcards

1
Q

Heparin Directly Activates

A

platelets, factor XII, complement, neutrophils, monocytes (aka: immune, inflammatory, complement systems)

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2
Q

HIT

A

heparin-induced thrombocytopenia and thrombosis

heparin binds to PF4 and makes IgG antibodies= decrease platelets by 50%

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3
Q

On Bypass and quick exposure of blood to ECC

A

-plasma protein adsorption to ECC surface
-contact activation of blood (coag/complement/cell signaling stimulation-XII, C3, platelets)
-emboli formation 1)surgery (wound debris) 2)blood activation 3) homologous bld (if not filtered) 4) crystalloid solution 5) roller/spallation
-increased interstitial fluid/edema
=====Whole body inflammation and Temp organ dysfunction

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4
Q

Inflation Response Spectrum

A
(varies patient to patient)
1- mild= fever and leukocytosis
2- significant= tachycardia, high CO/O2 consumption/perm, low SVR
3- Organ dysfunction
4- multiple organ dysfunction 
5- death
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5
Q

Key Players: 5 Protein Systems

A

Contact Activation, Intrinsic , Extrinsic Coag, Fibrinolysis, Complement

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6
Q

Heparin Directly Effects/Stimulates

A

platelets, factor XII, complement, neutrophils, monocytes

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7
Q

Protein on Tubing Stimulates

A

platelets, factor XII, complement

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8
Q

Contact Activation Stimulates

A

complement, coagulation

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9
Q

Plasma Contact Activations Involves 4 Proteins

A

factor XII, prekallikrein, HMWK, factor XI

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10
Q

Intrinsic Coagulation Initiated by

A

plasma contact activation with ECC because of Factor XII (along with HMWK and kallikrein)
(inside vessels)

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11
Q

Extrinsic Coagulation Initiated by

A

Tissue Factor exposure- converse IX and X to IXa and Xa

outside vascular

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12
Q

Thrombin Actions

A

produces fibrin, activates platelets, stimulates tPA

fibrinolysis extrinsic: tPA, fibrin/ intrinsic: XIIa, HMWK, kallikrein

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13
Q

Complement System

A

innate system
classical (antigen-antibody complex)
alternative (C3b, terminal pathway feedback, contact, plasmin)
terminal (C3 convertase)
–end product prevent/limit damage from antigen

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14
Q

Complement End Products

A
  • opsonization and phagocytosis (C3b, C4b)
  • lysis= MAC (C5b, 6-9)
  • agglutination= antigens adhere to each other
  • neutrolize virus
  • chemotaxis (C5a- call neutrophil and macrophages)
  • activates mast and basophils (C3a, C4a, C5a)
  • inflammation= increase perm/dilation, decrease CO
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15
Q

C Factors= anaphylactic

A

C3a, C4a, C5a (dilates, mast/basophils, inflammation)

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16
Q

C Factors= chemotaxis neutrophil, monocytes, endothelial cells

A

C5a

17
Q

C Factors= opsonization

A

C3b, C4b

neutrophil and macrophages come eat!

18
Q

Key Players: 5 Cells

A

platelets, neutrophils, monocytes, lymphocytes, endothelial cell
(please not my little eel)

19
Q

Platelet: early, late activation and response

A

early activation- EEC contact, heparin, thrombin!
late activation- C5b-9, hypothermia, hemodilution, sheer force, cytokines
response to activation (change in shape)= express GPIIb/IIIa (fibrin), secrete P-selectin receptor (mono and neutrophils)

20
Q

Neutrophils

A

C5a, kallikrein, XIIa, heparin, MAC

  • express MAC and L-selectins (rolling)
  • MAJOR role in reperfusion injury
21
Q

Monocyte

A

C5a, thrombin, bradykinin at wound or injury

- takes longer than neutrophils

22
Q

Lymphocytes response

A

decrease numbers after CPB= increase chance for infections

23
Q

Endothelial Cell Activates

A

(C5a, thrombin, cytokines)

-extrinsic coag, vasodilator, fibrinolysis, inflammatory, perm

24
Q

How can we control Blood-Surface interface

A

1) surface bound heparin
2) surface modifications
3) blood modifications (colloid prime, corticosteroids, TXA, platelets, NO)
4) pump modifications (cent vs roller, mini circuit, ultrafiltration)

25
Q

Surface Modifications (hep vs non hep coated)

A

Hep= carmela, trillium, bioline (with albumin)

No Hep= x-coating, balance biosurface, soft line (with albumin), phisio