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Pharm II MHM - Exam 2 > STEMI Lecture > Flashcards

STEMI Lecture Flashcards

1
Q

What is the recommended anti-platelet therapy for Class I NSTE-ACS patients?

A

ASA

  • Use clopidogrel if ASA intolerant/allergic
  • Use a GP IIb/IIIa inhibitor if cath and PCI planned (max tx = 8 days)
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2
Q

What is the recommended anti-platelet therapy for Class IIa NSTE-ACS patients?

A
  • Use GP IIb/IIIa inhibitor in high risk pts if invasive strategy NOT planned
  • Use a GP IIb/IIIa inhibitor in pts receiving clopidogrel if cath and PCI planned
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3
Q

What is the recommended anti-platelet therapy for Class IIb NSTE-ACS patients?

A

Use a GP IIb/IIIa inhibitor in low risk pts when PCI NOT planned

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4
Q

What is the recommended anti-platelet therapy for Class III NSTE-ACS patients?

A

Use abciximab in pts when PCI is NOT planned

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5
Q

Why is anti-platelet therapy essential in ACS?

A

Prevents thrombosis from plaque rupture

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6
Q

Chewing aspirin tablets inhibits platelets ___ faster

A

50%

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7
Q

162 mg daily of aspirin completely inhibits:

A

COX-1

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8
Q

325 mg daily of aspirin is max effective dose for ____

A

TXA2 inhibition

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9
Q

Peak serum concentration of aspirin occurs within:

A

1-2 hours

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10
Q

How do NSAIDs and aspirin interact?

A
  • Compete for same receptor
  • NSAIDs block and prevent acetylation
  • Space these 3 hours apart
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11
Q

Why is aspirin held for 6 hours after CABG and 24 hours after thrombolytics?

A

Prolonged wound healing

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12
Q

What is clopidogrel and what does it do?

A
  • Thienopyridine

- Selective irreversible inhibition of ADP-mediated platelet activation (cold, shear stress)

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13
Q

Clopidogrel binds ___ but has no effect on ____

A
  • P2Y12 and P2Y1 receptors

- No effects on TXA2, PGI2

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14
Q

Which anti-platelet has extensive hepatic metabolism?

A

Clopidogrel

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15
Q

Activity of clopidogrel is reduced by:

A

PPIs and other potent CYP219 inhibitors

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16
Q

Clopidogrel has reduced bioactivation in which population?

A

Persons of Chinese ancestry

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17
Q

How is clopidogrel used after coronary stent placement?

A

With ASA for up to 1 year

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18
Q

What is ticlopidine?

A
  • Irreversible thienopyridine P2Y12 inhibitor

- Clopidogrel/prasugrel now replaces this

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19
Q

How does dipyridamole work?

A
  • Inhibits adenosine deaminase and PDE

- Allows cAMP and adenosine accumulation and vasodilation

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20
Q

How does cilostazol work?

A
  • Inhibits PDE 3
  • Increases cAMP
  • Allows vasodilation
  • Inhibits vascular SMC proliferation
  • Inhibits platelets
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21
Q

How do GP IIb/IIIa inhibitors work?

A
  • Typically the receptors bind fibrin, thrombin, vWF
  • Allows for adhesion, activation, aggregation of platelets
  • Blocking the receptors prevents clotting
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22
Q

How does eptifibatide work?

A
  • Selective, reversible, competitive GP IIb/IIIa inhibition

- Temporarily blocks fibrin cross-linking

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23
Q

When should you be cautious with eptifibatide?

A
  • PTT 45+ secs

- CrCl less than 50

24
Q

When should you be cautious with tirofiban?

A
  • Platelets less than 150K
  • PTT 45+ secs
  • CrCl less than 30
25
Q

What is abciximab and how does it work?

A
  • Mouse monoclonal antibody
  • GP IIb/IIIa inhibitor
  • Binds and dissociates rapidly
26
Q

What is a major ADE to be aware of with abciximab?

A

Hypersensitivity reactions from infusion

27
Q

What type of compound is Heparin?

A

Sulfated mucopolysaccharide

28
Q

Where is endogenous heparin found?

A

Mast cells

29
Q

LMWH favors inhibition of which factor?

A

Xa

30
Q

How do sodium and calcium heparin relate?

A

They are bioequivalent

31
Q

What is the half life of heparin anticoagulation?

A

1.5 hours

32
Q

How is heparin eliminated?

A

Transported to reticuloendothelial system, phagocytized

33
Q

When can heparin resistance occur?

A
  • Hepatic cirrhosis
  • Nephrotic syndrome
  • DIC
34
Q

What is the therapeutic concentration of heparin?

A

0.2 to 0.4 U/mL via protamine titration with aPTT of 1.5-2.5x control

35
Q

Which populations have highest occurrence of bleeding complications with heparin?

A
  • Renal failure

- Elderly women

36
Q

Who is at highest risk to developing HIT?

A

Surgical patients

37
Q

When does peak anti-Xa activity of Enoxaparin occur?

A

Within 3-5 hours

38
Q

What is dalteparin?

A

LMWH ranging from 3000-8000 daltons

39
Q

When does peak anti-Xa activity of Dalteparin occur?

A

Within 2-4 hours

40
Q

When is Fondaparinux used?

A
  • STEMI pts receiving fibrinolytics

- NSTEMI PCI or conservative treatment

41
Q

When is Fondaparinux contraindicated?

A
  • CrCl less than 30

- Wt less than 50 kg

42
Q

When should Fondaparinux be stopped prior to CABG or surgery?

A
  • 24 hours prior

- Switch to heparin

43
Q

What kind of compound is Bivalirudin and how does it work?

A
  • 20 AA synthetic direct thrombin inhibitor
  • Analogue to a natural 65 AA thrombin inhibitor
  • Binds catalytic site on thrombin
  • Temporarily prevents soluble and clot-bound thrombin interactions
44
Q

When should fibrinolytics be given in acute STEMI?

A

Within 30 minutes (if PCI within 90 mins is not possible)

45
Q

When should fibrinolytics be used?

A

STEMI only

46
Q

How are fibrinolytics reversed?

A

Aminocaproic acid

47
Q

What kind of compound is Alteplase and how does it work?

A
  • Serine protease
  • Cleaves Arg-Val bond in plasminogen, converting it to plasmin
  • Plasmin degrades fibrin
48
Q

What is Alteplase less active on?

A

Systemically circulating plasminogen

49
Q

Alteplase is given with which other meds?

A

Heparin, enoxaparin

50
Q

How is Alteplase administered?

A

Infused over 1.5 - 3 hours

51
Q

What is reteplase?

A
  • Fibrinolytic

- Recombinant deletion mutant of wild type tissue plasminogen activator

52
Q

What happens when reteplase is given?

A
  • Early platelet inhibition (w/in 6 hours)

- Rebound platelet aggregation (at 24 hours) with increased GP IIb/IIIa expression

53
Q

What inactivates reteplase in the blood?

A
  • C1 inactivator
  • a1 antitrypsin
  • a2 antiplasmin
54
Q

What is tenecteplase?

A
  • Fibrinolytic
  • Genetically re-engineered alteplase
  • 2 AA, 4 alanine substitutions
  • Produced in Chinese hamster ovary cells
55
Q

How is tenecteplase inactivated in the blood?

A

By PAI-1

*Extensive inactivation in the liver

56
Q

Which fibrinolytic has a biphasic half-life?

A

Tenecteplase

57
Q

Which anti-platelet acts by REVERSIBLE inhibition?

A

Ticagrelor

Pharm II MHM - Exam 2 (5 decks)

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