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Therapeutics 2 Exam 4 -Geriatric, Coagulation > Thrombolytic Drugs > Flashcards

Thrombolytic Drugs Flashcards

1
Q

What is the role of plasmin?

A

Degrades the fibrin clot and clears in from the blood vessel

(Fibrinolysis and clot degradation)

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2
Q

What does the fibrinolytic pathway do?

A

Dissolves a blood clot after the blood vessel has healed

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3
Q

What is the mechanism of action of thrombolytics?

A

Increase the conversion of plasminogen to plasmin

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4
Q

What is the function of plasmin?

A

Degrades fibrin and dissolves clots

*digests fibrin and fibrinogen

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5
Q

What enzyme activates plasminogen to plasmin?

A

t-PA or u-PA

*what we target to break down clots

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6
Q

What does PAI-1 do?

A

bind t-PA or u-PA and inhibits activity

(prevents activation of plasminogen to plasmin)

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7
Q

What does a2AP do?

A

Degrades plasmin

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8
Q

What does TAFI do?

A

Prevents plasmin from binding fibrin which inhibits fibrinolysis

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9
Q

How does t-PA work?

A

Cleaves the arg-val bond to activate plasminogen to plasmin

(serine protease)

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10
Q

What does a2-antiplasmin do?

A

Inactivates plasmin

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11
Q

What is t-PA inhibited by?

A

PAI-1 and PAI-2

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12
Q

What are the indications for thrombolytic therapy?

A

-Acute MI
-Acute ischemic thrombotic stroke
-PE

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13
Q

What is the standard of care acute myocardial infarction (MI)?

A

STENT placement

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14
Q

What are the two types of STENTs?

A

Bare-metal

Drug-coated

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15
Q

What is the purpose of drug-coated STENTs

A

Drugs prevent restenosis (when an artery opened through a medical procedure re-narrows)

-by inhibiting smooth muscle cell proliferation
-increase risk of subsequent thrombosis

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16
Q

What is the structure/ function of Alteplase?

A

-Recombinant human t-PA

527 amino acid residues

*Binds fibrin to activate plasminogen

17
Q

What is the structure/function of Reteplase?

A

-Recombinant human t-PA with deletion of aa (355/527)

**More potent
**Faster onset

*Lacks fibrin binding domain, less fibrin-specific than alteplase

18
Q

What is the structure/ function Tenecteplase?

A

-Recombinant, mutant form of t-PA

*Longer half-life
*Given by single IV bolus

*More fibrin specific than t-PA

19
Q

What domains in Alteplase and Tenecteplase are part of fibrin binding?

A

Finger

Kringle 1/2

20
Q

What are the mutations present in tenecteplase?

A

-Increased half-life

-Reduced inhibition by PAI

-Enhanced activity at thrombi

21
Q

What is the mechanism of action of alteplase, reteplase, and tenecteplase?

A

Tissue Plasminogen Activator (t-PA)

22
Q

What tPA is the target of alteplase and tenecteplase?

A

tPA bound to a fibrin clot

23
Q

What tPA is the target of reteplase?

A

tPA in the plasma OR bound to a fibrin clot

24
Q

How are tissue plasminogen factors administered?

A

IV

25
Q

What is the duration of actions of the tissue plasminogen activators?

A

Alteplase: 5-10min
Reteplase: 13-16min
Tenecteplase: 90-130min

26
Q

What are the adverse effects of tissue plasminogen activators?

A

-Bleeding
-internal bleeding
-Superficial or surface bleeding

(can dissolve more than just the targeted clot)

27
Q

What are anti-fibrinolytic agents used for?

A

-To stop bleeding caused by thrombolytic drugs

-Adjunct therapy in hemophilia

-re-bleeding from intracranial aneurysms

28
Q

How do anti-fibrinolytic agents work?

A

-Plasmin binds fibrin through a lysine binding site to activate fibrinolysis

-Drugs act as a lysine analog to bind receptor on plasminogen and plasmin

-Results in block of plasmin binding to target fibrin

29
Q

What are the anti-fibrinolytic drugs?

A

Aminocaproic acid

Tranexamic acid

Lysine

30
Q

Which anti-fibrinolytic drug is most potent?

A

Tranexamic acid

(10x more potent than aminocaproic acid_

31
Q

What are the risks associated with anti-fibrinolytic agents?

A

Intravascular thrombosis formation as a result of fibrinolysis inhibition

Thrombi formed during therapy are not easily lysed

Therapeutics 2 Exam 4 -Geriatric, Coagulation (8 decks)

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