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FPC2 Exam 7 > ACS and angina > Flashcards

ACS and angina Flashcards

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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
Prasugrel is contraindicated in?
stroke or TIA | avoid upstream loading
26
Ticagrelor is contraindicated? What are AEs?
contraindicated in patients with ICH. | Dyspnea, bradyarrhythiias, there is mortality benefit vs clopidogrel
27
What is the MOA of cangrelor and why is it special?
potent, rapidly reversibly, intravenous, P2Y12 inhibitor. | PK: onset within 2 minutes and returns to normal platelets within 1 hr
28
When would you use cangrelor?
adjunct to PCI in patients who haven't gotten P2y12 inhibitor and are not being given GP IIb/IIIa
29
What is the mechanism of Glycoprotein IIb/IIIa inhibitors?
block final common pathway of platelet aggregation-> inhibit cross linking of platelets by fibrinogen bridges
30
What are the available glycoprotein IIb/IIIa inhibitors
eptifibatide (integrilin) | tirofiban (aggrastat)
31
When is glycoprotein IIb/IIIa inhibitors indicated
adjunct at time of PCI if high thrombus burden and inadequate P2Y12. use when heparin chosen as anticoagulant. not much benefit after DAPT
32
________ anticoagulation is recommended for all patients with ACS
parenteral | use for >2 days, up to 8 days or until PCI
33
Which anticoagulants are IV and which are SQ?
unfractionated heparin and bivalirudin (IV) | enoxaparin and fondaparinux (SQ)
34
MOA of β blockers
competitively inhibit β-1 adrenergic receptors | lower HR, contractility, BP, oxygen demand
35
Precautions/AEs for β blockers
HF, low output, cariogenic shock. Brady cardia/heart block, active asthma or reactive airway disease (use CCB)
36
Which two early hospital therapies should be started for patients coming in from a ACS besides anti platelets + anticoagulants?
β blockers, ace inhibitors
37
MOA of ace-inhibitors
inhibit angiotensin I to angiotensin II (vasoconstrictor)-> reduce afterload, BP, neurohormonal activation
38
AEs for ACE inhibitors
hypotension, renal failure, hyperkalemia, pregnancy, angioedema, cough
39
Angiotensin receotpro blockers MOA
displace angiotensin II from AT1 receptor-> BP lower, aldosterone release lower
40
AEs of angiotensin receptor blockers
similar to ACE inhibitors except cough. | reduced incidence of angioedema
41
What are two β blockers
metoprolol | carvedilol
42
What are 3 ACE-inhibitors
lisinopril, captopril, ramipril
43
What are 3 angiotensin receptor blockers
valsartan, losartan, candesartan
44
Additional secondary prevention therapies for ACS besides β blockers, ACE inhibitors, ARB
statin, aldosterone antagonists
45
MOA of Statins? What are some adverse effects
Inhibits HMG-CoA reductase (rate limiting for cholesterol synthesis) AEs: hepatotoxicity, myopathy/rhabdomyolysis drug interactions
46
MOA and AEs for aldosterone antagonists
compete with aldosterone for receptor sites in distal renal tubes (K+ sparing, blocks effects on arteries smooth muscle) hyperkalemia, renal impairment, gynecomastia
47
What are two aldosterone antagonists?
spironolactone | eolerenone
48
What to use in someone with stable ischemic heart disease (Pharma wise)?
ASA 81mg, moderate high intensity statin, ace inhibitors/ARBs symptom: antianginals
49
What are first line, second line, and third line anti-anginals?
1st: β blockers (tolerability is ? bc fatigue, sexual dysfunction sleep problems) 2nd: CCB, nitrates 3rd: ranolazine
50
What are dihydropyridine and nondihydropyridine calcium channel blockers?
DHP: amlodipine, felodipine, nifedipine | non-DHP: diltiazem, verapamil
51
How to calcium channel blockers work?
limit Ca2+ ion influx in L type Ca chennels-> smooth muscle relax-> improve myocardial oxygen supply-> decrease o2 demand from reduce contractility/HR
52
Calcium channel blockers can be used in lieu of _____ or as an _____
β blocker | add on therapy
53
You can be on ACE inhibitor or ___ but not both
angiotensin receptor blockers
54
What are the drugs of choice for prinzmetal's or vasospastic angina?
calcium channel blockers
55
If there is LV dysfunction or conduction disease, ____ is the preferred therapy
DHP
56
What are adverse effects of DHP and non-DHP
Both: hypotension, peripheral edema | Non-DHP: bradycardia/heart block, worsening HF, constipation (verapamil?diltiazem)
57
What is the MOA of nitroglycerin
formation of nitric oxide activates guanylate cyclase-> cyclic GMP-> smooth muscle relax-> coronary *vasodilation* + blood redistribution-> lower preload-> reduce myocardial oxygen demand
58
For nitroglycerin, observe daily intervals of _______ to_______
``` nitrate free (10-14hr) avoid development of tolerance. titrate to use lowest dose possible ```
59
what are adverse effects of nitroglycerin
*headache*, flushing, hypotension, reflex tachycardia
60
What is the big AE of statins
muscle pain
61
What are contraindications for nitroglycerin
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
What is MOA of ranolazine
inhibit late inward sodium current during ischemic conditions-> improve ventricular diastolic tension and o2 consumption minimal effect on HR and BP
63
Ranolazine is used when
symptomatic relief of chronic angina
64
What are AEs of ranolazine
constipation, nausea, dizziness, headache, QT prolongation
65
Why would you use aldosterone antagonists
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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