2. Fibrinolytics Flashcards

1
Q

ASA is an effective treatment across the entire spectrum of ACS. (T/F)

A

True

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2
Q

What is the goal of ASA therapy in ACS?

A

quickly block formation of TXA2 in platelets

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3
Q

What is the effective acute dose of ASA?

A

160 - 325 mg

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4
Q

Why is the low dose ASA (81mg) ineffective in ACS?

A

takes several days to achieve full antiplatelet effect

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5
Q

Why is the ASA chewed in ACS?

A

buccal and sublingual absorption rather than GI

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6
Q

What is the ACS general treatment acronym and what does it stand for?

A

O: oxygen
M: morphine
N: nitroglycerin
A: antiplatelet

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7
Q

Why is pain management an important element of ACS treatment?

A

pain leads to increased SNS activity which increases the heart rate and leads to more ischemia

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8
Q

What analgesic agents are used with AMI?

A
  • morphine
  • Meperidine
  • Pentazocine
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9
Q

What is the analgesic agent of choice with ACS?

A

morphine

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10
Q

Why is morphine the agent of choice for ACS?

A

it has venodilatory effects that reduce ventricular preload

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11
Q

What organic nitrate agent is indicated in most ACS?

A

sublingual nitroglycerin - patient must be conscience

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12
Q

Why are organic nitrates indicated in ACS?

A
  • enhances cardiac blood flow by coronary vasodilation

- decreases ventricular preload

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13
Q

What patients are contraindicated for sublingual NG?

A
  • hypotension (SBP < 90)

- especially accompanied by bradycardia

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14
Q

After administering sublingual NG, what should be monitored?

A

BP

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15
Q

What is the goal of using beta-blockers in ACS?

A

reducing infarct size

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16
Q

Which AMI patients are most suited for beta-blocker therapy?

A

sinus tachycardia and HTN

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17
Q

Why are AMI patients who have sinus tachycardia and HTN suitable for BB therapy?

A
  • BBs lower HR and BP

- reduce myocardial O2 demand

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18
Q

What AMI patients are contraindicated for BB therapy?

A
  • HF

- Hypotension/bradycardia

19
Q

What BB agent is preferred in ACS and why?

A

metoprolol because it is cardio-selective

20
Q

What is the goal of therapy for using fibrinolytics in ACS?

A

remove unwanted fibrin thrombi

21
Q

What stimulates the endothelium to release t-PA?

A

reduced flow when thrombi occlude vessels

22
Q

Released t-PA has a relatively long half-life. (T/F)

A

False: rapidly cleared from blood or inhibited by plasminogen activator inhibitors

23
Q

Plasmin that leaves the clot is inhibited by what?

A

alpha 2-antiplasmin

24
Q

Describe the t-PA 90 minute administration

A
  • 15 mg IV bolus
  • 0.75 mg/kg (50 mg max) over 30 minutes
  • 0.5 mg/kg (35 mg max) over 60 minutes
25
Q

t-PA is rapidly deactivated; why do we administer it?

A

Pharmacological administration of plasminogen activators overwhelms the inhibition

26
Q

What is the first generation fibrinolytic agent?

A

streptokinase

27
Q

What produces streptokinase?

A

beta-hemolytic streptococci

28
Q

Streptokinase has high intrinsic enzymatic activity. (T/F)

A

False: no intrinsic enzymatic activity

29
Q

Streptokinase forms a stable, non-covalent 1:1 complex with what?

A

plasminogen

30
Q

Streptokinase is not fibrin specific. (T/F)

A

True

31
Q

What is the MOA of streptokinase?

A

Complexes with plasminogen to expose active sight and cleave into plasmin which goes on to degrade fibrin.

32
Q

Why can streptokinase administration not be repeated?

A

antibodies develop after treatment

33
Q

What is the second generation fibrinolytic agent?

A

rt-PA : alteplase

34
Q

What is the key fibrinolytic feature of ateplase?

A

prolonged plasma clearance

35
Q

What are the third generation fibrinolytic agents?

A
  • derivatives of t-PA
  • rPA : reteplase
  • TNK-t-PA : tenecteplase
36
Q

Reteplase lacks domains that increase elimination by the _______.

A

liver

37
Q

Reteplase has a ______ affinity for fibrin than t-PA.

A

lower

38
Q

Why is reteplase thought to be more effective than t-PA?

A

it is hypothesized that it can penetrate the clot and “chew it up” from the inside

39
Q

Why is tenecteplase thought to be more effective than t-PA?

A

It is 80x more resistant to plasminogen activator inhibitor-1 than t-PA.

40
Q

How is tenecteplase dosed?

A

single IV bolus (weight based) over 5 seconds

41
Q

Tenecteplase is more fibrin-specific than t-PA. (T/F)

A

True

42
Q

What is anistreplase?

A

complex of protein bound streptokinase

43
Q

What is the thrombolytic activity of anistreplase?

A

release of the streptokinase component