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FPC2 Exam 7 > ACS and angina > Flashcards

ACS and angina Flashcards

1
Q

The two types of ischemic heart disease

A

stable ischemic heart disease

acute coronary syndrome

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2
Q

Three types of acute coronary syndrome

A

unstable angina
NSTEMI
STEMI

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3
Q

Everyone that presents with heart problems should get what

A

aspirin

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4
Q

What at the two options for repercussion therapy

A 
Cath lab (PCI-> balloon open the artery and place stent)
Fibrinolytic therapy
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5
Q

Reperfusion therapy should be administer to all patients within symptom onset _____

A

less than 12 hours

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6
Q

The preferred method of reperfusion therapy is

A

Primary PCI

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7
Q

Limitations of fibrinolysis includes

A 
time dependent efficacy, normalized blood flow in 50-60% (90% in PCI)
recurrence
hemorrhagic
lack of angiography
limited patient candidacy
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8
Q

What is the mechanism of fibrinolytic therapy?

A

plasminogen is converted to plasmin by the tPA or other drugs. this breaks down gelatin, casein, and fibrin

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9
Q

What are two of the most commonly used fibrinolytic therapies. what are max doses

A

tenecteplase (TNFase) 50mg
alteplase (activase) 100mg
(both are a bolus)

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10
Q

What would a reason for giving fibrinolytic over PCI?

A

timing. want to do pci as early as literally humanly possible

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11
Q

What are some absolute fibrinolytic contraindications

A

prior intracranial hemorrhage, stroke in last 3 months, head trauma, vascular lesion, aortic dissection, cns surgery, intracranial neoplasm, active bleeding, uncontrolled HTN

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12
Q

Regardless of reperfusion stragetgy they all get _____

A

2nd anti-platelet agent
therapeutics anticoagulation
2˚-> statins, β blockers, ace inhibitor, aldosterone

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13
Q

NSTEMI- two different strategies and their components

A

conservative: antiplatelet + anticoagulation
invasive: anti-platelet -> PCI + anticoagulation

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14
Q

What are the 3 antiplatelets

A

aspirin
P2Y12 inhibitor
glycoprotein IIb/IIIa inhibitor

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15
Q

What are the 4 anticoagulants

A

unfractionated heparin (UFH)
low molecular weight heparins (LMWH)
direct thrombin inhibitors (DTIs)
direct factor Xa inhibitors

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16
Q

What is DAPT

A

dual anti-platelet therapy

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17
Q

What is the MOA of aspirin

A

antiplatelet-> irreversibly inhibits COX1 and 2 enzymes -> reduce TXA2-> 7-8 days

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18
Q

Adverse effects of aspirin and what to do about it

A 
hypersensitivity (substitute clopidogrel)
active bleeding (GI ulcer)
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19
Q

Aspirin should be used with an oral ______ for at least a year in patients with ACS

A

P2Y12

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20
Q

What is MOA of P2Y12 inhibitors?

A

block P2Y12 component of ADP receptor on platelet surface-> reduces platelet aggregation

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21
Q

What are P2Y12 inhibitors?

A

clopidogrel (plavix), prasugrel (effient), ticagrelor (Brilinta),

Less used cangrelor and kengreal

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22
Q

Inhibition of platelet aggregation of the different P2Y12 inhibitors?

A

clopidogrel: 50%
prasugrel: 70-75
ticagrelor: 70-75

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23
Q

What is special about clopidogrel and metabolism? when is it the preferred p2y12 inhibitor?

A

variable because genetic polymorphisms of cyp2c19

preferred with concurrent need for long term AC (afib)

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24
Q

How long do you need to wait for someone on p2y12 inhibitors to get surgery?

A

hold it for 5-7 days

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25
Q

Prasugrel is contraindicated in?

A

stroke or TIA

avoid upstream loading

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26
Q

Ticagrelor is contraindicated? What are AEs?

A

contraindicated in patients with ICH.

Dyspnea, bradyarrhythiias, there is mortality benefit vs clopidogrel

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27
Q

What is the MOA of cangrelor and why is it special?

A

potent, rapidly reversibly, intravenous, P2Y12 inhibitor.

PK: onset within 2 minutes and returns to normal platelets within 1 hr

28
Q

When would you use cangrelor?

A

adjunct to PCI in patients who haven’t gotten P2y12 inhibitor and are not being given GP IIb/IIIa

29
Q

What is the mechanism of Glycoprotein IIb/IIIa inhibitors?

A

block final common pathway of platelet aggregation-> inhibit cross linking of platelets by fibrinogen bridges

30
Q

What are the available glycoprotein IIb/IIIa inhibitors

A

eptifibatide (integrilin)

tirofiban (aggrastat)

31
Q

When is glycoprotein IIb/IIIa inhibitors indicated

A

adjunct at time of PCI if high thrombus burden and inadequate P2Y12.
use when heparin chosen as anticoagulant.
not much benefit after DAPT

32
Q

________ anticoagulation is recommended for all patients with ACS

A

parenteral

use for >2 days, up to 8 days or until PCI

33
Q

Which anticoagulants are IV and which are SQ?

A

unfractionated heparin and bivalirudin (IV)

enoxaparin and fondaparinux (SQ)

34
Q

MOA of β blockers

A

competitively inhibit β-1 adrenergic receptors

lower HR, contractility, BP, oxygen demand

35
Q

Precautions/AEs for β blockers

A

HF, low output, cariogenic shock. Brady cardia/heart block, active asthma or reactive airway disease (use CCB)

36
Q

Which two early hospital therapies should be started for patients coming in from a ACS besides anti platelets + anticoagulants?

A

β blockers, ace inhibitors

37
Q

MOA of ace-inhibitors

A

inhibit angiotensin I to angiotensin II (vasoconstrictor)-> reduce afterload, BP, neurohormonal activation

38
Q

AEs for ACE inhibitors

A

hypotension, renal failure, hyperkalemia, pregnancy, angioedema, cough

39
Q

Angiotensin receotpro blockers MOA

A

displace angiotensin II from AT1 receptor-> BP lower, aldosterone release lower

40
Q

AEs of angiotensin receptor blockers

A

similar to ACE inhibitors except cough.

reduced incidence of angioedema

41
Q

What are two β blockers

A

metoprolol

carvedilol

42
Q

What are 3 ACE-inhibitors

A

lisinopril, captopril, ramipril

43
Q

What are 3 angiotensin receptor blockers

A

valsartan, losartan, candesartan

44
Q

Additional secondary prevention therapies for ACS besides β blockers, ACE inhibitors, ARB

A

statin, aldosterone antagonists

45
Q

MOA of Statins? What are some adverse effects

A

Inhibits HMG-CoA reductase (rate limiting for cholesterol synthesis)
AEs: hepatotoxicity, myopathy/rhabdomyolysis
drug interactions

46
Q

MOA and AEs for aldosterone antagonists

A

compete with aldosterone for receptor sites in distal renal tubes (K+ sparing, blocks effects on arteries smooth muscle)
hyperkalemia, renal impairment, gynecomastia

47
Q

What are two aldosterone antagonists?

A

spironolactone

eolerenone

48
Q

What to use in someone with stable ischemic heart disease (Pharma wise)?

A

ASA 81mg, moderate high intensity statin, ace inhibitors/ARBs
symptom: antianginals

49
Q

What are first line, second line, and third line anti-anginals?

A

1st: β blockers (tolerability is ? bc fatigue, sexual dysfunction sleep problems)
2nd: CCB, nitrates
3rd: ranolazine

50
Q

What are dihydropyridine and nondihydropyridine calcium channel blockers?

A

DHP: amlodipine, felodipine, nifedipine

non-DHP: diltiazem, verapamil

51
Q

How to calcium channel blockers work?

A

limit Ca2+ ion influx in L type Ca chennels-> smooth muscle relax-> improve myocardial oxygen supply-> decrease o2 demand from reduce contractility/HR

52
Q

Calcium channel blockers can be used in lieu of _____ or as an _____

A

β blocker

add on therapy

53
Q

You can be on ACE inhibitor or ___ but not both

A

angiotensin receptor blockers

54
Q

What are the drugs of choice for prinzmetal’s or vasospastic angina?

A

calcium channel blockers

55
Q

If there is LV dysfunction or conduction disease, ____ is the preferred therapy

56
Q

What are adverse effects of DHP and non-DHP

A

Both: hypotension, peripheral edema

Non-DHP: bradycardia/heart block, worsening HF, constipation (verapamil?diltiazem)

57
Q

What is the MOA of nitroglycerin

A

formation of nitric oxide activates guanylate cyclase-> cyclic GMP-> smooth muscle relax-> coronary vasodilation + blood redistribution-> lower preload-> reduce myocardial oxygen demand

58
Q

For nitroglycerin, observe daily intervals of _______ to_______

A 
nitrate free (10-14hr)
avoid development of tolerance. titrate to use lowest dose possible
59
Q

what are adverse effects of nitroglycerin

A

headache, flushing, hypotension, reflex tachycardia

60
Q

What is the big AE of statins

A

muscle pain

61
Q

What are contraindications for nitroglycerin

A

RV failure, aortic stenosis, hypertrophic obstructive cardiomyopathy
recent use of phosphodiesterase inhibitors (sildenafil, tadalafil)
(any condition that is preload dependent to maintain cardiac output)

62
Q

What is MOA of ranolazine

A

inhibit late inward sodium current during ischemic conditions-> improve ventricular diastolic tension and o2 consumption
minimal effect on HR and BP

63
Q

Ranolazine is used when

A

symptomatic relief of chronic angina

64
Q

What are AEs of ranolazine

A

constipation, nausea, dizziness, headache, QT prolongation

65
Q

Why would you use aldosterone antagonists

A

post MI without significant renal dysfunction who are getting ACE inhibitors and β blockers and have and LVEF<40% and DM or symptomatic HF

FPC2 Exam 7 (4 decks)

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