Thrombolytics + extra (STEMI/NSTEMI/UA) Flashcards

1
Q

Thrombolytics

A

Alteplase
Reteplase
Tenecteplase

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

Thrombolytics Indications

A

PCI within 90 minutes door to balloon time

Lytics within 30 minutes if PCI within 90 minutes is impossible-door to needle time

Hemodynamically compromised pts (cardiogenic shock, pulm edema, congestion) receiving lytics to receive angiography and PCI

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

Thrombolytics MOA

A

lytics dissolve pathologic thrombus and fibrin at sites of vascular injury:

  • endogenous tissue plasminogen activator (t-PA) released from endothelium
  • plasminogen converted to plasmin
  • plasmin digests clot bound fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lytics can be used in ____ but not ___ or __

A

use lytics in STEMI ONLY***!!!!!

DO NOT USE IN UA/NSTEMI

  • NOT better when added to ASA, clopidogrel, anticoag, and GP IIB/IIIA inhibitors
  • actually will increase risk of MI and other serious hemorrhagic events ☹
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Lytics Considerations

A

New and improved lytics are based on endogenous t-PA

structures make each unique: Finger and Kringle pieces an effect fibrin specificity, potency, clearance etc

alteplase is more like tenecteplase but overall all 3 have same efficacy!

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

Lytics reversal?

A

Lytics CAN be reversed with AMINOCAPROIC ACID ☺

  • binds to lysine on plasminogen and plasmin
  • prevents interaction with fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alteplase MOA

A

Serine protease cleaves Arg-Val bond in plasminogen and converts it to plasmin
*Requires fibrin as cofactor for activation of plasminogen
-enhanced proteolysis in presence of clot fibrin, highly specific for clot bound fibrin
No direct antiplatelet effects

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

Alteplase indication

A

Given with UFH or enoxaparin

LESS active on systemically circulating plasminogen

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

Alteplase Metabolism

A

Non antigenic

  • moderate degree of fibrin depletion and D dimmer accumulation
  • peak thrombolytic effects within 30-60 minutes, IV infusion required to maintain lysis

75% achieve patency within 90 minutes
>50% achieve TIMI grade 3 flow

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

Alteplase clearance

A

Degraded into component amino acids in liver
-50% of alteplase cleared within 5 minutes of stoping infusion, 80% in 10 minutes

half life 27-46 minutes

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

Alteplase CI/ Precautions

A
CI:
-bleeding
-uncontrolled htn*****
-av malformation or aneurysm
-HX/evidence of hemorrhagic stroke
-SAH
-Platelets less than 100,000
Heparin w/in 48 hours 
precautions: recent trauma, high bleed risk, recent punctures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Alteplase considerations

A

Replaced streptokinase bc of fibrin secificty

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

Recteplase MOA

A

Catalyzes conversion of plasminogen to plasmin and enhances thrombolysis

Early platelet inhibition within 6 hrs with rebound platelet aggregation at 24 hrs with increased GP IIb/IIIa expression

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

Recteplase indications

A

Given with UFG, enoxaparin

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

Recteplase Metabolism

A
Peak response within 30-90 min of IV
-60-70% achieve patency by 90 minutes
-60% with TIMI grade 3 flow
inactivated in blood by:
-C1 inactivator
-a-1 antitrypsin
-a-2 antiplasmin
RENAL clearance
Half life 13-16 minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Recteplase CI/precautions

A

CI:

  • bleeding
  • av malformation or aneurysm
  • recent surgery/trauma
  • hx of CVA; **uncontrolled HTN
    precautions:
  • recent punctures, surgery, trauma, antiplatelet tx
  • recent GI/GU bleeding
  • Advanced age; high bp
17
Q

Recteplase considerations

A

Recombinant deletion mutant of wild type tissue plasminogen activator

  • does not have kringle-1, finger, GF domains
  • decreased fibrin specificity, higher potency, shorter half life
18
Q

Tenecteplase MOA

A

Plasma inactivation via PAI-1

19
Q

Tenecteplase Indications

A

Used with UFH, enoxaparin

20
Q

Tenecteplase Metabolism

A

Extensive inactivation in the liver

Half life: biphasic—24 minutes then 115 minutes ****
75% achieve patency at 90 minutes
60% TIMI 3 flow

21
Q

Tenecteplase CI/precautions

A

CI:

  • bleeding
  • av malformation or aneurysm
  • recent surgery/trauma
  • hx of CVA; uncontrolled HTN**
    precautions:
  • recent punctures, surgery, trauma, antiplatelet tx
  • recent GI/GU bleeding
  • Advanced age; high bp >180/110
22
Q

Tenecteplase SE

A

Increased half life
Increased fibrin specificity
Reduced inactivation by plasminogen activation inhibitor 1 (PAI-1)

 decrease risk by lowering infusion rate!! **

23
Q

Tenecteplase considerations

A

Genetically reengineered alteplase ()
-has 2 AA substitutes and 4 alanine substitutes

produced in Chinese hamster ovary cells

24
Q

Pathogenesis to MI

A

Plaque disruption/fissure/erosion
thrombosis formation
Non ST elevation ACS or ST elevation ACS

25
What % pts with ACS have >= 2 plaques
50%
26
TIMI Risk Score
``` more increased needs a more aggressive TX Age >/= 65 >/= 3CAD risk factors Prior Coronary Stenosis >50% ST deviation >/=2 Anginal events in less than 24 hours ASA last 7 days elevated cardiac markers ```
27
Class 1 agents for NSTE-ACS
-Aspirin Clopidogrel if allerigic Or use with clopidogrel if invasive approach is not planned Stop clopidogrel 5-7 days before CABG or surgery -Use GP IIb/IIIa inhibitor if cardiac cath and PCI is planned- max tx 8 days
28
Class 2a Agents for NSTE-ACS
Use GP IIb/IIIa inhibitor in pts RECEIVING CLOPIDOGREL if cardiac cath and PCI planned Use GP IIb/IIIa inhibitor in high risk pts if invasive strategy is not planned
29
Antiplatelet tx functions to
prevent thrombosis from plaque rupture in ACS
30
Dual or Tripple antiplatelet therapy can reduce odds of vascular caused death, MI or stroke by
22%
31
What anti platelet combos are there?
ASA + Clopidogrel (one or both) option to add GP IIb/IIIa inhibitors caution because increase risk to bleed