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Perf tech III > test 5 > Flashcards

test 5 Flashcards

1
Q

Clot strength

A
  • Platelets 80%-90%

* Fibrin 10%-20%

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2
Q

Component Measurements:
PT/INR:
PTT:

A
  • PT/INR: measures extrinsic clotting (VIIa, Xa, IIa)
  • PTT: measures intrinsic clotting (XIIa, XIa, IXa, IIa)
  • Fibrinogen concentration
  • Platelet Count (doesn’t tell you function of platelets)
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3
Q

What is thromboeleastography (TEG)

A
  • A whole blood hemostasis analyzer

* Point of care test

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4
Q

How does TEG work

A
  • Cup oscillates • Pin is attached to torsion wire
  • Clot binds pin to cup
  • Degree and magnitude of pin motion are functions of the clot kinetics and mechanical properties
  • System generates a hemostasis profile
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5
Q

TEG parameters: R

Likely variable

A
  • Reaction time (time to clot formation)

- Likely variable: Coagulation factors

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6
Q

TEG parameters: Alpha

A
  • Speed of fibrin accumulation

- Likely variable: Fibrinogen

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7
Q

TEG parameters: K

A
  • Time elapsed until clot reaches a fixed strength

- Likely variable: Fibrinogen

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8
Q

TEG parameters: MA

A
  • Highest vertical amplitude of TEG tracing

- Likely variable: Platelets

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9
Q

TEG parameters: LY30

A
  • % of amplitude reduction 30 minutes after its maximum

- Likely variable: fibrinolysis

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10
Q 
Elongated R - Thrombin formation abnormalities
1. Possible cause of
imbalance?
2. Possible Etiologies?
3. Common Treatments?
A 
Possible cause of
imbalance:
        • Slow enzymatic reaction
Possible Etiologies
        • Factor deficiency/dysfunction
        • Residual heparin
Common Treatments:
        • FFP
        • Protamine
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11
Q 
Low alpha angle - Fibrinogen abnormalities
1. Possible cause of
imbalance?
2. Possible Etiologies?
3. Common Treatments?
A

Possible cause of imbalance
• Slow rate of fibrin formation
Possible etiologies
• Low fibrinogen levels or function
• Insufficient rate/amount of thrombin generation
• Platelet deficiency/dysfunction
Common Treatments
• FFP
• Cryoprecipitate

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12
Q 
Low MA - Platelet function abnormalities
1. Possible cause of
imbalance?
2. Possible Etiologies?
3. Common Treatments?
A 
Possible causes:
        • Insufficient platelet-clot formation
Possible etiologies
        • Poor platelet function
        • Low platelet count
        • Low fibrinogen levels or function
Common treatments:
        • Platelets
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13
Q 
High MA - Platelet function abnormalities
1. Possible cause of
imbalance?
2. Possible Etiologies?
3. Common Treatments?
A 
Possible causes:
        • Excessive platelet activity
Possible etiologies
        • Platelet hypercoagulability
Common Treatments
        • Antiplatelet agents
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14
Q

Pictures of possible tracings

A
  • Look at them
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15
Q

TEG assays - Standard (kaolin)

A
  • Use normal parameters
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16
Q

TEG assays - Rapid TEG

A
  • Uses tissue factor and kaolin to activate extrinsic and intrinsic pathways
  • R-value is replaced by TEG-ACT value
  • Other parameters the same
  • Increased speed can save valuable time
17
Q

TEG assays - Heparinase

A

• Used on bypass or post bypass alongside a standard TEG

18
Q

TEG assays - Platelet Mapping

A
  • Determines to what degree platelet function is inhibited due to pharmacological inhibition of either the arachidonic acid (AA) or adenosine diphosphate (ADP) pathways
    * AA: Aspirin
    * ADP: Clopidogrel
    * Run alongside a standard TEG and a TEG with added AA or ADP.
    * Calculates the percentage of inhibition relative to the patient’s maximum platelet function
19
Q

What drugs are monitored during platelet mapping

A
  • Antiplatelet Drugs
    * ADP receptor inhibitors
    * Examples: clopidogrel, ticlopidine
    * Arachidonic acid pathway inhibitors
    * Example: aspirin
    * GPIIb/IIIa inhibitors
    * Examples: abciximab, tirofiban, eptifibatide
20
Q

Why platelet mapping

A
  • Individual response to antiplatelet drugs determines clinical outcome
  • Knowing percent of platelet inhibition is insufficient to determine therapeutic efficacy
  • Knowledge of maximum platelet function is also required as a reference point
21
Q

Rotational Elastometry (ROTEM)

A
  • STATIONARY CUP, ROTATING SPINDLE
  • Clot impedes rotation of the pin
  • Additional tests available
22
Q

Sonoclot

A

• Viscoelastic detection system
• Provides information on the entire hemostatic process
• Generates a qualitative graph and quantitative results
- Tells you
-coagulation, formation of the fibrin network, clot retraction, and the breakdown of the clot
- helps determine if it’s a coagulation issue or if there is a bleeder
• Tubular probe oscillates up and down within a blood sample
• Senses resistance to motion that the probe encounters through various stages of hemostasis
- slightly faster than other 2
- fibrinolysis takes longer to be determined

23
Q

Sonoclot graph

A
  • Clot evolution saved as a graph

* Clot signal value versus time

24
Q

Sonoclot Liquid Phase

A

• Ends when the viscosity of the sample begins to increase with thrombin generation and the resulting initial fibrin formation

25
Q

Sonoclot fibrin gel formation

A
  • Once thrombin forms, the fibrinogen converts to fibrin

* Fibrin spontaneously polymerizes into a fibrin gel

26
Q

Sonoclot clot retraction

A
  • Occurs when platelets function normally
  • Platelets adhere to nodes of the fibrin gel and cause the gel to collapse together or retract
  • As the clot retracts, it tightens
27
Q

Sonoclot time to peak

A
  • The faster the time to peak, the greater the platelet function
  • Sharp, well defined peaks infication strong retraction
  • Dull, poorly defined peaks indicate weak retraction

Perf tech III (55 decks)

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