Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CV Perf Tech II > Blood Surface Interactions (Part 1) - Exam 3 > Flashcards

Blood Surface Interactions (Part 1) - Exam 3 Flashcards

1
Q

How does heparin work?at

A

No direct inhibition of coag; accelerates action of antithrombin
Direct activation of other blood components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What blood components does heparin activate?

A 
Platelets
Factor XII
Complement system
Neutrophils
Monocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What allergic response can occur from heparin?

A

HIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

HIT

A

Heparin Induced Thrombocytopenia

Causes bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What percent of patients receiving heparin develop HIT?

A

2-5% of patients receiving heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HITT

A

Heparin Induced Thrombocytopenia and Thrombosis

causes thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What percent of patients develop HITT?

A

0.1-0.2% of patients receiving heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the mechanism for HIT and HITT?

A

Heparin binds to PF4 and induces IgG formation

Heparin/PF4-IgG complex activates plts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PF4

A

Platelet factor 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the formation of heparin/PF4-IgG result in?

A

Decreases circulating number of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HIT is defined as what percent decrease in platelets?

A

40-50% decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does HITT involve?

A

Decrease in number of platelets and any evidence of thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does quick exposure of whole blood mass to biomaterials of ECC result in?

A

Plasma protein adsorption on to surface of ECC
Contact activation of blood
Emboli formation
Increased Interstitial fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How fast does plasma protein adsorption onto the surface of ECC occur?

A

Very quick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does the amount of plasma proteins absorbed onto ECC depend on?

A
  1. Protein and intrinsic surface activity of biomaterial
  2. Wettability
  3. Hydrophilic/ hydrophobic ratio
  4. Surface chemistry
  5. surface electrical properties
  6. roughness/ porosity
  7. subsurface features
  8. distribution of function receptor sites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does activation of blood correlate with?

A

Physical/Chemical properties of biomaterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Is plasma protein adsopriton onto surface of ECC predictable?

A

No; correlation is made retrospectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does contact activation of blood to ECC stimulate?

A

Coagulation cascade
Complement system
Alteration of cell signaling substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Contact activation of blood to ECC exposes receptor sites for what?

A

Blood cells
Plasma proteins (FXII, Complement protein 3)
Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Surgery Emboli Formation Sources: Wound Debris

A 
Fibrin
Fat
Calcium
Cellular debris
Other foreign material
Air emboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Surgery Emboli Formation Sources: Surgical Manipulation

A 
Plaque debris (arterial cannulation, XC)
Air emboli (cannulation, incomplete deairing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Blood Activation/Trauma Emboli Formation Sources

A

Fibrin emboli
Macroaggregates of proteins and lipoproteins
Fat flobules
Platelet and Leukocyte aggregates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Homologous Blood (unfiltered) Emboli Formation

A

Platelet & Leukocyte aggregates
Fibrin
Lipid precipitates
red cell debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Crystalloid Solutions: emboli formation

A

Inorganic debris

dust

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Roller Pumps: Emboli Formation
Spallation
26
Embolic Material
``` Fibrin Fat (Free/denatured lipoproteins/chlyomicrons) Denatured protein Platelet aggreagtes Leukocyte aggregates Red cell debris Gas (Nitrogen, oxygen) Foreign material (Ca, Tissue debris, sutures) Spallated material ```
27
What type of fats can be embolic material?
Free fat denatured lipoproteins Chylomicrons
28
Chylomicrons
a droplet of fat present in the blood or lymph after absorption form the small intestine
29
What is the accumulation of interstitial fluid proprotional to?
Duration of bypass
30
What can cause increased interstitial fluid?
Increased capillary permeability
31
CPB can result in
Whole Body Inflammation | Temporary Organ Dysfunction
32
What are the Five Protein Systems
``` Contact Activation System Intrinsic Coagulation System Extrinsic Coagulation System Fibrinolysis Complement Activation ```
33
What are the four proteins involved with plasma contact activation?
Factor XII Prekallikrein HMWK Factor XI
34
What does FXII do when activated by contact with ECC?
Adsorbed onto foreign surface of ECC | Changes shape produces active protease FXIIa and XIIf
35
What must be present for FXII to be adsorbed onto foreign surface of ECC?
Prekallikrein and HMWK
36
What does active protease FXIIa do?
1. Cleaves prekallikrein to kellikrein 2. Cleaves HMWK to bradykinin 3. Activates FXi to FXIa
37
What is a strong neutrophil agonist?
Kallikrein
38
What is a weak neutrophil agonist?
FXIIa
39
What must be present for FXIIa to activate FXI to FXIa?
Kallikrein and HMWK must be present
40
What does FXIa do?
Activates intrinsic coagulation cascade; results in thrombin production
41
How is the intrinsic coagulation cascade initiated?
Plasma contact activation; initiated directly by blood contact with the ECC
42
How is the exntrinsic coagulation cascade initiated?
By the expression of tissue factor on nonvascular cells
43
What are the 2 forms of tissue factor?
1. Cell bound tissue factor | 2. Soluble plasma tissue factor
44
What does tissue factor do?
Binds to and activates FVII; which activates FX
45
What are the actions of thrombin?
Production of fibrin from fibrinogen Cross-linking fibrin Activating platelets Stimulating the production of tissue plasminogen activator (t-PA) by endothelial cells
46
How many proteins are involved in the complement system?
30+ proteins; most inactive enzyme precursors
47
What pathways are involved in the complement system?
Classical Pathway Alternative pathway Terminal Pathway
48
How is the classical pathway of the complement system activated?
Antigen-antibody complexes
49
How is the alternative pathway of the complement system activated?
C3b (a produce of classical pathway) | Inititated by spontaneous activation on a continuous basis
50
What is alternative pathway
A feedback loop for amplification
51
What is the terminal pathway in the complement system?
Classical and alternative merge at the level of C3 convertase production
52
What do the end products of the complement system do?
Work to prevent/ limit damage from invading organism or toxins
53
How does the end produce membrane attack complex work to prevent damange from invading organism?
``` Opsonization Lysis Agglutination Neutralization of viruses Chemotaxis Activation of mast cells and basophils Inflammation ```
54
Describe opsonization.
Neutrophils and macrophages activated | They engulf bacterial to which antigen-antibody complex is attached
55
Describe Lysis.
Final product called lytic complex or terminal complement complex. Creates a pore in the cell membrane of bacteria or other invading organisms that allows the influx of ions and water into the cell
56
Describe agglutination
Complement produces change surface of invading organisms; organisms adhere to each other
57
Neutralization of viruses
Products can attack structures of some viruses and render them non-virulent
58
What causes chemotaxis of neutrophils and macrophages?
C5a
59
What happens during chemotaxis?
Large number of phagocytes migrate to the area
60
What are mast cells nad basophils activated by?
C3a, C4a, C5a
61
What do mast cells release?
Histamine and other substances into local fluids
62
What does activation of mast cells and basophils result in?
Increased local blood flow and increased leakage of fluid and protein into the tissue
63
What does inflammation result in?
INcreased capillary permeability Altered vasomotor tone Impaired cardiac function
64
What does the activation of classical and alternative pathway result in?
``` Cellular damange Endothelial and leukocyte activation Histamine release Increased vascular permeability Generalized inflammatory response Platelet activation ```
65
What 4 things initiate the classical pathway?
Surface contact activation of FXII Heparin-protamine Complexes Ischemia reperfusion Blood-air interface
66
What 3 things activate the alternative pathway?
Contact with foreign surface Activated pericardium and suction blood Ischemia reperfusion
67
What activates complement system?
Classical and alternative pathways
68
What are 3 anaphylatoxins with vasoactive properties?
C3a, C4a, C5a
69
What is a major neutrophil agonist?
C5a
70
What results in opsonization?
C3b, C4b
71
What does the terminal complement complex do?
Accelerates thrombin formation via action on prothrombinase complex Activates platelets

CV Perf Tech II (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions