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Pharm II MHM - FINAL > STEMI > Flashcards

STEMI 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
What is abciximab and how does it work?
- Mouse monoclonal antibody - GP IIb/IIIa inhibitor - Binds and dissociates rapidly
26
What is a major ADE to be aware of with abciximab?
Hypersensitivity reactions from infusion
27
What type of compound is Heparin?
Sulfated mucopolysaccharide
28
Where is endogenous heparin found?
Mast cells
29
LMWH favors inhibition of which factor?
Xa
30
How do sodium and calcium heparin relate?
They are bioequivalent
31
What is the half life of heparin anticoagulation?
1.5 hours
32
How is heparin eliminated?
Transported to reticuloendothelial system, phagocytized
33
When can heparin resistance occur?
- Hepatic cirrhosis - Nephrotic syndrome - DIC
34
Which populations have highest occurrence of bleeding complications with heparin?
- Renal failure | - Elderly women
35
Who is at highest risk to developing HIT?
Surgical patients
36
When does peak anti-Xa activity of Enoxaparin occur?
Within 3-5 hours
37
What is dalteparin?
LMWH ranging from 3000-8000 daltons
38
When does peak anti-Xa activity of Dalteparin occur?
Within 2-4 hours
39
When is Fondaparinux used?
- STEMI pts receiving fibrinolytics | - NSTEMI PCI or conservative treatment
40
When is Fondaparinux contraindicated?
- CrCl less than 30 | - Wt less than 50 kg
41
When should Fondaparinux be stopped prior to CABG or surgery?
- 24 hours prior | - Switch to heparin
42
What kind of compound is Bivalirudin and how does it work?
- 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
43
When should fibrinolytics be given in acute STEMI?
Within 30 minutes (if PCI within 90 mins is not possible)
44
When should fibrinolytics be used?
STEMI only
45
How are fibrinolytics reversed?
Aminocaproic acid
46
What kind of compound is Alteplase and how does it work?
- Serine protease - Cleaves Arg-Val bond in plasminogen, converting it to plasmin - Plasmin degrades fibrin
47
What is Alteplase less active on?
Systemically circulating plasminogen
48
Alteplase is given with which other meds?
Heparin, enoxaparin
49
How is Alteplase administered?
Infused over 1.5 - 3 hours
50
What is reteplase?
- Fibrinolytic | - Recombinant deletion mutant of wild type tissue plasminogen activator
51
What happens when reteplase is given?
- Early platelet inhibition (w/in 6 hours) | - Rebound platelet aggregation (at 24 hours) with increased GP IIb/IIIa expression
52
What inactivates reteplase in the blood?
- C1 inactivator - a1 antitrypsin - a2 antiplasmin
53
What is tenecteplase?
- Fibrinolytic - Genetically re-engineered alteplase - 2 AA, 4 alanine substitutions - Produced in Chinese hamster ovary cells
54
How is tenecteplase inactivated in the blood?
By PAI-1 | Extensive inactivation in the liver
55
Which fibrinolytic has a biphasic half-life?
Tenecteplase
56
Which anti-platelet acts by REVERSIBLE inhibition?
Ticagrelor

Pharm II MHM - FINAL (17 decks)

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