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Cardio Exam 2 > 22 - Thrombolytic Therapy > Flashcards

22 - Thrombolytic Therapy Flashcards

1
Q

What are the two pathways of the coagulation cascade?

A

The extrinsic and intrinsic pathway

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2
Q

What is the goal of both the extrinsic and intrinsic pathways?

A

The extrinsic and intrinsic pathways serve to activate factor X to Xa, a component of the prothrombinase complex (enzyme)

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3
Q

What does the activated prothrombinase enzyme complex do?

A

Converts prothrombin (factor II) into thrombin (factor IIa)

Thrombin is a vital part of a clot and causes a reduction in blood loss

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4
Q

How does thrombin increase clot formation?

A

Thrombin activates factor XIII into factor XIIIa, which stabilizes the fibrin clot by cross-linking fibrin

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5
Q

What system balances the clotting cascade?

A

The fibrinolytic system

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6
Q

What is the main player in the fibrinolytic system?

A

The conversion of plasminogen to plasmin results in the breakdown of fibrin clots

tPA or tissue plasminogen activator serves as the enzyme which activates plasminogen into plasmin

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7
Q

Describe the relationship between clotting and clearing

A

Both are necessary, but both must be controlled

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8
Q

What agents are used to prevent the formation or growth of clots?

A
  • Warfarin
  • Aspirin (ASA)
  • NOACs
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9
Q

What agents are used to breakdown already formed clots

A

Thrombolytics

  • These agents are plasmin activators
  • Plasmin is an agent within the body which has a direct lytic effect on fibrin clots
  • You are not giving the patient plasmin, but rather you are activating theirs
  • This means that thrombolytics are not direct lytics, but rather indirect lytics through the activation of plasmin
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10
Q

What are the thrombolytic agents we use to breakdown already formed clots?

A
  • Streptokinase
  • Anisolyated plasminogen-strptokinase activator complex (APSAC)
  • Urokinase
  • Tissue plasminogen activator
  • New plasminogen activators
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11
Q

Describe streptokinase as a treatment option for the breakdown of already formed clots

A
  • Derived from Group C streptococci
  • Directly activates plasminogen into plasmin
  • It is antigenic meaning the body responds to it because it is a pathogen
  • It is effective in MI time-dependent treatment by using drip dosing
  • On WHO list of essential medications
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12
Q

Describe APSAC as a treatment option for the breakdown of already formed clots

A

Anisolyated plasminogen-streptokinase activator complex (APSAC)

  • Contains plasminogen waiting to be activated by hydrolysis reactions within the body
  • Compounded in vitro (out of the body) but activated in vivo (inside the body)
  • Antigenic with repeated use
  • Anaphylaxis reactions are rare but possible
  • Easy to use bolus dosing
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13
Q

Describe urokinase as a treatment option for the breakdown of already formed clots

A
  • Derived from human neonatal kidney cells meaning they are non-antigenic (great feature)
  • Directly activate plasminogen into plasmin
  • Currently used quite a bit
  • Used to clear lines (PE, direct arterial infusion)
  • Limited use in coronary thrombosis
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14
Q

Describe tPA as a treatment option for the breakdown of already formed clots

A

Tissue plasminogen activator

  • AKA Alteplase
  • Directly activates plasminogen into plasmin
  • A recombinant molecule which is originally extracted from human material
  • tPA naturally occurs in the blood
  • tPA was the drug of choice for acute MI and is now a generic drug
  • Now there are new versions of this drug
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15
Q

Describe new plasminogen activators as a treatment option for the breakdown of already formed clots

A
  • All are given via IV bolus dosing (“drip-and-ship”)
  • There are three: reteplase, tenecteplase, lanoteplase
  • They are pretty much “me-too” drugs which change something small and market big
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16
Q

What is reteplase made from?

A
  • Recombinant DNA E. coli culture

- It is now a generic (price drop)

17
Q

What is tenecteplase made from?

A
  • Modified native tPA

- It is currently recommended by the AHA for acute MI***

18
Q

What is lanoteplase made from?

A
  • Chinese hamster ovary cell cultures

- Not currently used

19
Q

When attempting to treat an MI via thrombolysis, what are the two main categories of goals?

A

Disease-oriented goals

  • Get good blood flow to infarcted vessels
  • Reduce the infarct size measured by a reduced level of markers in blood samples

Patient-oriented goals

  • Improved survival rate
  • Reduce left ventricle failure, ventricular dysrhythmias, direct complications of MI (myocardial rupture, mural thrombi, etc.)
20
Q

Describe the goal of getting good blood flow to infarcted vessels

A

Use the TIMI grading scale
- Kind of confusing because there is a TIMI risk score and a TIMI flow score - they contradict

TIMI flow

  • It is a quantification of the amount of flow that a vessels is getting
  • TIMI flow = 0, no blood flow
  • Lows score is bad
  • Want to get TIMI flow to a 3 in an MI

TIMI risk

  • It is a quantification of risk of complications of MI
  • TIMI risk = 0, no risk
  • Low score is good

TIMI flow does not equal TIMI risk

21
Q

What constitutes a “high risk” patient when treating MI?

A

A group at risk for mortality following MI

  • Hypotensive patients (pump failure)
  • Diabetic patients

Remember that when treating with thrombolytic therapy, you need to assess risk vs. harm. In the case of high risk groups, their risk of dying is very high so there is more to gain by treating with thrombolytics.

22
Q

What groups have a decreased rate of mortality following acute MI?

A

Young patients

They may not benefit as much from thrombolytic therapy, but you will still consider the risk/reward balance

23
Q

What group has been shown to have more head bleeds following thrombolytic therapy with acute MI?

A

Older patients

Need to balance out risk of harm and risk of benefit

24
Q

What are the two main complications of thrombolytic therapy?

A
  • Bleeding

- Allergic reactions

25
Q

Describe the risk of bleeding from thrombolytic therapy

A
  • Lytics don’t know what specifically to lyse
  • Bleeding is most often minor (at IV sites, etc.)
  • Intracranial bleeds occur in 1%
26
Q

What is the typical patient which suffers from an intracranial bleed following thrombolytic therapy?

A
  • Older than 65
  • Less than 70 kg
  • Initially poorly contorlled hypertension
  • Use of tPA as a thrombolytic
  • Less risk of intracranial bleed with streptokinase
27
Q

How common are allergic reactions of thrombolytic therapies?

A

Allergic reactions are rare with streptokinase and others in the streptokinase family

28
Q

What patients would be at high risk of death if you elect to NOT use thrombolytic therapy to treat their acute MI (delay risk)?

A

High risk of death in…

  • Advanced age
  • Female
  • Reduced L ventricular function
  • Anterior MI
  • Bundle branch block (BBB)
  • Marked ST elevation
  • Diabetes
  • Pulse 100+
  • Systolic BP less than 100
  • Long delay since onset of symptoms
29
Q

What are the two different sets of protocols that exist for acute MI or acute coronary syndrome?

A
  • Protocol for when symptoms began less than 120 minutes (2 hours) ago
  • Protocol for when symptoms began more than 120 minutes (2 hours) ago
30
Q

What is the protocol for ACS/AMI when it began less than 2 hours ago?

A
  • First contact cath lab for PCI (Percutaneous Coronary Intervention)
  • Aspirin, nitro, morphine/tentanyl
  • Oxygen if needed
  • Local choice of anticoagulant (heparin, enoxaparin, ticagrelor)
  • Possibly clopidogrel, atorvastatin
31
Q

What is the protocol for ACS/AMI when it began more than 2 hours ago?

A
  • Thrombolysis
  • TNKase recommended by AHA (a type of tPA)
  • Aspirin, nitro, morphine/fentanyl
  • Heparin or enoxaparin
  • Maybe clopidogrel or atorvastatin
32
Q

When an acute MI presents late, what do you do? (4-12 hours)

A
  • Consider using lytics such as streptokinase

- PCI (Percutaneous Coronary Intervention at cath lab) is less useful and more dangerous

33
Q

When an acute MI presents late, what do you do? (12+ hours)

A
  • Will possibly present with ongoing symptoms and necrosis

- Only use lytic therapy with a large MI in patients with a low CVA risk (cerebrovascular accident)

34
Q

What do you NEED to remember about thrombolytisc?

A
  • Thrombolytics are NOT anticoagulants
  • Thombolytics activate a natural process
  • Thrombolytics have benefits and risks - they usually go bi-directionally meaning patients with the most risk benefit the most, so they tolerate the harm)
  • More newer lytics have no great patient-level benefit
  • Administering lytics in acute MI when PCI (Percutaneous Coronary Intervention) is delayed will save lives

Cardio Exam 2 (12 decks)

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