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Flashcards in Pharm - ACS Deck (37)
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1
Q

What is the goal of therapy for a patient with UA or NSTEMI?

A
  • prevent progression to STEMI and death
  • prevent ischemia and life-threatening ventricular arrhythmias
  • relief of ischemic pain
  • prevent further thrombosis of or embolism from an ulcerated plaque
2
Q

For a patient presenting with UA (or any ACS), what is the correct aspirin product to use? and the dose?

A
  • chewable, uncoated aspirin
  • 162-325 mg ASAP
  • continued indefinitely
3
Q

MoA of aspirin in treating UA/NSTEMI

A
  • in cytosol AA (arachadonic acid) is converted to 2 prostaglandin intermediates by COX-1 and COX-2
  • COX-1 is essential for synthesis of thromboxane A2 (TxA2)
  • TxA2 stimulates platelet aggregation and vasoconstriction
  • aspirin blocks COX-1, reducing production of TxA2 = decreased platelet aggregation

(flow chart on pg 6 if needed)

4
Q

appropriate dosing of sublingual nitroglycerin for UA

A
  • 3 sublingual nitroglycerin tabs 0.4 mg

- one at a time, spaced 5 min apart

5
Q

MoA of nitroglycerin

A
  • nitrates enter vascular smooth muscle and form NO
  • NO stimulate an enzyme to form cGMP which does 2 things:
  • inhibits Ca++ entry into cell (relaxation)
  • causes downstream dephosphorylation of myosin = relaxation = vasodilation

(flow chart on pg. 7 if needed)

6
Q

ADRs of sublingual nitro

A
  • HA (intense) and flushing
  • SL tingling
  • postural hypotension
  • occasional nausea
  • tachycardia
7
Q

ADRs of aspirin

A

(Letassy didn’t have specific list in packet)

  • chewing aspirin can irritate mouth, make sure to rinse
  • takes 7 days to reverse so stop 1 week before procedure to prevent bleeding
8
Q

define the term cardioselectivity in context of a cardioselective beta blocker

A
  • refers to the ability of a drug to preferentially block the B-1 receptor
  • cardioselective beta blockers have the potential advantage of less likely to cause bronchoconstriction or peripheral vasodilation
  • the selectivity is usually lost at higher doses
  • best one is metroprolol tartrate**
9
Q

define dual antiplatelet therapy (DAPT)

A
  • all patients w/ NSTEMI should be treated w/ aspirin and a P2Y12 receptor blocker (ASA + P2Y12RB)
  • it’s directed at limiting platelet adhesion and aggregation (early steps of coronary a. thrombus formation)
  • it has been shown to significantly reduce the risk of cardiovascular death, nonfatal MI or stroke
10
Q

what is the recommended duration of DAPT for patients w/ stent placement secondary to UA/NSTEMI

A
  • at least 12 months

- unless high bleed risk

11
Q

What are the P2Y12 receptor blockers? (the 4 that letassy gave us)

A
  • clopidogrel (Plavix)
  • prasugrel (effient)
  • ticagrelor (brilinta)
  • cangrelor (Kengreal)
12
Q

MoA of clopidogrel (Plavix)

A
  • P2Y12 ADP receptor inhibitor
  • requires 2 steps for biotransformation to active metabolite
  • irreversibly blocks the P2Y12 portion on the ADP receptor on platelet surface
  • reduced platelet aggregation
13
Q

MoA of ticagrelor

A
  • noncompetitive, reversible, P2Y12 receptor antagonist
  • reversibly binds to ADP receptors on platelet surface
  • prevents ADP-mediated platelet activation and aggregation
14
Q

In treating a patient with UA, what is the appropriate dose of clopidogrel?

A
  • **Loading dose: 300-600 mg

- followed by 75 mg orally daily

15
Q

In treating a patient with UA, what is the appropriate dose of prasugrel?

A
  • **loading dose: 60 mg
  • followed by 10mg orally daily
  • 5mg daily if used in pts w/ high bleeding risk
16
Q

In treating a patient with UA, what is the appropriate dose of ticagrelor?

A
  • **Loading dose: 180 mg

- followed by 90 mg orally BID given w/ low dose ASA

17
Q

In treating a patient with UA, what is the appropriate dose of cangrelor?

A
  • IV bolus 30 mcg/kg prior to PCI

- followed by infusion (4 mcg/kg/min) continued for at least 2 hrs or duration of PCI

18
Q

In treating a patient with UA, what is the appropriate dose of unfractionated heparin?

A
  • **loading dose: IV bolus 60-70 units/kg (MAX 5000 units)

- followed by 12 units/kg/hr or until aPTT goal is achieved

19
Q

In treating a patient with UA, what is the appropriate dose of LMWH?

A
  • no loading dose

- 1 mg/kg subQ q 12

20
Q

ADRs of clopidogrel

A
  • bleeding (but less than aspirin)

- neutropenia

21
Q

drug-drug interactions of clopidogrel

A
  • it is an inactive prodrug requiring transformation by liver CYP3A and 2C19
  • significant drug interaction:
  • PPIs
  • Statins
22
Q

explain what can occur with the drug interactions of clopidogrel

A
  1. PPIs: may decreases serum concentrations of active metabolites; increases risk of decreasing effectiveness of clopidogrel; avoid
  2. statins: may diminish the antiplatelet effect of clopidogrel
23
Q

ADRs of ticagreglor

A
  • bleeding
  • dyspnea** (unique):
  • usually occurs in 1st week
  • may be transient or persistant
  • not linked to a deterioration in heart or lung function
24
Q

drug drug interactions of ticagrelor

A
  • it inhibits CYP3A4 so can increase serum concentrations of some drugs
  • stronger CYP3A4 inhibitors can increase levels of ticagrelor and reduce speed of onset
  • it reversibly inhibits platelet activation
25
Q

black box warning for prasugrel

A

bleeding and TTP

26
Q

contraindications for prasugrel

A
  • 75 or older w/o high risk of sent thrombosis
  • hx of prior stroke or TIA
  • active or suspected bleeding
27
Q

which antiplatelet agents are pro drugs?

A
  • clopidogrel

- prasugrel

28
Q

what are the anticoagulant agents?

A
  • IV UFH
  • LMWH
  • direct thrombin inhibitors
29
Q

MoA of UFH

A
  • catalyzes the inactivation of thrombin and Xa
  • prevents conversion of fibrinogen to fibrin and clot formation
  • indirect thrombin inhibitor
30
Q

MoA of LMWH

A
  • inactivates Xa but w/ lesser effect on thrombin
  • doesn’t prolong aPTT
  • indirect thrombin inhibitor
31
Q

MoA of fondaparinux (anticoag)

A

-selective inhibitor of Xa

32
Q

MoA of bivalirudin (anticoag)

A

-reversible direct thrombin inhibitor

33
Q

Given a pt w/ UA/NSTEMI and renal insufficiency, what is the appropriate anticoag?

A
  • UFH

- b/c it’s not cleared by kidneys

34
Q

Given a patient with STEMI, what is the appropriate time interval of admin of a fibrinolytic? and what is the expected benefit?

A
  • should be administered w/i 30 min of hospital arrival
  • benefit is greatest when administered w/i 2 hrs of symptom onset
  • significant benefit associated w/ admin up to 12 hrs from onset of chest pain
  • trend toward benefit when given 13-24hrs
35
Q

MoA of fibrinolytics

A

catalyze the conversion of plasminogen to plasmin which degrades fibrin

36
Q

indication of fibrinolytics in a pt w/ STEMI

A

-preferred agent if onset of sx is w/i 3 hrs and access to cardiac cath for PCI is delayed or unavailable

37
Q

MoA of glycoprotein IIb/IIIa blockers

A
  • bind to GP IIb/IIIa receptor

- causes conformational change that inhibits platelet aggregation