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PBL PY2 Fall > IHD Therapeutics Lecture 2 > Flashcards

IHD Therapeutics Lecture 2 Flashcards

1
Q

when a vulnerable atherosclerotic plaque ruptures, what 2 main things happen?

A
  1. activation of coagulation cascade

2. platelet adhesion, activation and aggregation

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2
Q

following plaque rupture and the activation of the coagulation cascade and platelet aggregation, what is formed?

A

a fibrin and platelet clot that occludes the coronary artery and could lead to myocardial infarction

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3
Q

define acute coronary syndromes

A

a spectrum of conditions resulting in myocardial ischemia after an acute thrombus causes a reduction in blood flow

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4
Q

list 3 characteristics of NSTE-ACS

A
  1. ST segment not elevated
  2. partial (platelet rich occlusion of coronary artery)
  3. can be ustable angina or NSTEMI depending on presence of cardiac biomarkers (similar presentation, but different severity)
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5
Q

List 4 characteristics of a STEMI

A
  1. ST elevation on ECG
  2. positive cardiac biomarkers
  3. total occlusion of coronary artery involving platelets and thrombin
  4. requires immediate coronary angiography and reperfusion
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6
Q

if a patient has the following presentation, what ACS would you suspect they may have? Chest pain described as “pressure”, occurs at rest or with minimal exertion, pain in the retrosternal area radiating to arma, neck, jaw, may have diaphoresis, SOB, nausea, abdominal pain, unexplained or new onset SOB on exertion, atypical symptoms like epigastric pain, indigestion, nausea, vomiting, fatique, syncope

A

either unstable angina or NSTEMI

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7
Q

if a patient presents with the following, what type of ACS would you suspect? Worsening pain/pressure in the chest described as “suffocating, squeezing, aching”, can presnt with less common atypical symptoms or silent unrecognized MI

A

STEMI

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8
Q

what objective findings suggest unstable angina?

A
  1. ST depression
  2. T wave inversion
  3. transient or non-specific ECG changes
  4. no positive biomarkers for cardiac necrosis
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9
Q

what are the objective findings for NSTEMI?

A
  1. ST depression
  2. T wave inversion
  3. transient or nonspecific ECG changes
  4. positive biomarkers (troponin elevation)
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10
Q

what are the objective findings for STEMI?

A
  1. ST elevation

2. positive troponin

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11
Q

what is the extent of injury for unstable angina?

A

no necrosis, partial occlusion of coronary artery

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12
Q

what is the extent of injury for NSTEMI?

A

myocardial injury, partial occlusion or coronary artery

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13
Q

what is the extent of injury in STEMI?

A

myocardial necrosis and total occlusion of the coronary artery

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14
Q

what are the goals for unstable angina?

A

prevent total occlusion
symptom control
risk factor modification

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15
Q

what are the goals for NSTEMI?

A 
prevent total occlusion
limit infarct site
control symptoms 
risk factor modification
reduce chest pain
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16
Q

what are the goals for STEMI?

A
  1. restore blood flow to the infarcted artery
  2. prevent complications (arrhythmias, death, thrombosis, bleeding)
  3. risk factor modification
  4. reduce pain
  5. restore normal ECG
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17
Q

why are women not as quickly diagnosed with ACS?

A

they are more likely to present with “atypical” symptoms and ECG changes are often not as clear in women

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18
Q

what is the preferred reperfusion technique?

A

PCI

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19
Q

for a STEMI how much time do you have from first medical contact (FMC) to PCI?

A

<120 minutes

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20
Q

when is fibrinolytic therapy indicated for STEMI?

A

if patient cant get PCI <120min

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21
Q

how long do you have from first medical contact to needle time for fibrinolysis?

A

30 min

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22
Q

if fibrinolysis is successful, patient needs to go for a PCI within ____(time) and if it fails, the patient needs to go for PCI within ____timeframe

A

24 hours; IMMEDIATELY

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23
Q

for treatment of NSTE-ACS, what 2 scores are used to determine patient risk and guide therapy?

A
  1. TIMI score

2. GRACE score

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24
Q

what is the goal time from FMC to procedure if the patient is diagnosed with STEMI in a PCI center?

A

90 min or less

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25
Q

what drugs should be used during the PCI prcedure?

A

anticoagulants like heparin, bivalrudin, or enoxaparin

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26
Q

what drusg should be avoided during PCI?

A
  1. routine use of GP 2b/3a inhibitors

2. IC lytics or IC adenosine

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27
Q

what is the default access site for PCI?

A

radial access

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28
Q

what are 7 complications of PCI?

A
  1. bleeding
  2. re-stensosis
  3. interventional complications like the dissection or rupture of the artery
  4. stent thrombosis
  5. contrast induced nephropathy
  6. arrhythmias
  7. mechanical complications like mitral regurgitation
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29
Q

how can contrast induced nephropathy be reduced?

A

IV fluids and hydration

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30
Q

what is the acronym for the adjunct treatment of STEMI (adjunct to revasularization)

A 
M-Morphine 
O-oxygen 
N-nitroglycerin
A-ASA
B-beta blocker
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31
Q

the canadian CV society recommends against O2 supplementation in patinets with O2 saturation of __% or greater

A

90

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32
Q

why is routine O2 supplementation not given for STEMI care unless O2 saturation is less than 90%?

A

O2 supplementation may result in anxiety, impaired communication and has no benefit if the patient is not hypoxic

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33
Q

why does the Canadian CV society advise against routine use of morphine for pain in STEMI patients?

A
  1. may mask pain that would indicate failed treatment

2. Inhibits gastric emptying which may cause vomiting (may vomit up oral antiplatelet therapy)

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34
Q

what is the infusion rate for nitroglycerin in hospital as adjunct to STEMI treatment?

A

10mcg/min and titrated to pain relief

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35
Q

in what situations should nitroglycerin not be given?

A
  1. SBP <90
  2. severe bradycardia (<50bpm)
  3. tachycardia (>100bpm)
  4. suspected RV infarction
  5. patients who have taken a PDE5 inhibitor
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36
Q

why is nitroglycerin C/i with PDE5 inhibitors?

A

causes life threatening hypotension

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37
Q

must wait ___hrs after sildenafil and vardenafil to give nitroglycerin

A

24

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38
Q

must wait ___hrs after tradalafil to give nitroglycerin

A

48

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39
Q

what is the MOA of ASA?

A

irreversible COX-1 inhibitor at low doses. Blocks the formation of thromboxane A2 and thromboxane platelet activation

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40
Q

what is the typical loading dose given to asa naive patients?

A

160-325mg

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41
Q

what formulation of ASA should be avoided as a loading dose? Why?

A

enteric coated bc of delayed and reduced absorption

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42
Q

what is the typical dose of ASA given to all patients?

A

81mg daily indefinitely (whether they had PCI or not)

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43
Q

ASA reduces the risk of death or MI by ___% compared to no antiplatelet therapy

A

50

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44
Q

which PGY12-i can be used for STEMI PCI?

A

clop, tica, prasu

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45
Q

which PGY12-i can be used for STEMI fibrinolysis?

A

clopidogrel

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46
Q

which PGY12-i can be used for NSTE-ACS PCI?

A

Clop, tica, prasu

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47
Q

which PGY12-i can be used for NSTE-ACS medical management?

A

clop and tica

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48
Q

ticagrelor dose fro DAPT

A

90mg BID

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49
Q

prasugrel dose for DAPT

A

10mg daily

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50
Q

clopidogrel dose for DAPT

A

75mg daily

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51
Q

if patients tolerate 1 year of DAPT treatment without risk of major bleeding, what should be done?

A

extend for up to 3 years

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52
Q

the PLATO study found what when comparing ticagrelor and clopidogrel in ACS for 1 year?

A

ticagrelor decreased risk of vascular death, MI, stroke, but increased bleeding and SOB

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53
Q

what were the results of the TRITON study that compared prasugrel vs clopidogrel in ACS + PCI for 14.5 months?

A

prasugrel decreased vascular death, MI, and stroke, but increased major bleeding

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54
Q

in most cases, which PGY12 inhibitors are recommended for DAPT?

A

ticagrelor and prasugrel over clopidogrel

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55
Q

why is prasugrel not recommended for DAPT in medical management?

A

due to the findings of the TRILOGY trial which compared prasugrel vs clopidogrel where prasugrel did not decrease vascular death, MI, or stroke

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56
Q

which trials are the basis for using clopidogrel for fibrinolytic DAPT?

A

CLARITY and TREAT trials

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57
Q

what are some examples of high risk features for thrombotic events?

A
  1. diabetes treated with PO hypoglycemics or insulin
  2. previous stent thrombosis
  3. smoking
    multiple stents or use of biodegradable vascualr scaffold
  4. Left main or proximal LAD stenting
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58
Q

what are some factors associated with increased bleeding risk?

A
  1. age >75
  2. anemia
  3. body weight <60kg
  4. regular use of NSAIDS or prednisone
  5. OAC therapy
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59
Q

what is stent thrombosis?

A

a life-threatening comlication after stent insertion

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60
Q

what is the most important predictor of stent thrombosis?

A

premature discontinuation of DAPT

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61
Q

mortality rate is as high as ___% in patients with stent thrombosis

A

45

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62
Q

what is the MOA of clopidogrel?

A

irreversible inhibitor of ADP-ediated platelet activation at P2Y12 receptor

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63
Q

is clopidogrel a parent drug or a pro-drug?

A

pro-drug

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64
Q

what type of prodrug os clopidogrel?

A

inactive thienpyridine prodrug

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65
Q

what is the loading dose of clopidogrel?

A

300mg

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66
Q

what PK factor needs to be accounted for when considering clopidogrel?

A

there are CYP2C19 polymorphisms that impact

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67
Q

what is the MOA of ticagrelor?

A

reversible P2Y12 inhibitor

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68
Q

what are the c/i for clopidogrel?

A
  1. active bleeding
  2. signoficant liver impairment
  3. use of repaglinide
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69
Q

what are the c/i of ticagrelor?

A
  1. active bleeding
  2. hx of intracranial hemorrhage
  3. moderate to severe hepatic impairment
  4. use of strong CYP3A4 inhibitors
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70
Q

what are the loading and regular doses of ticagrelor?

A

180mg (loading)

and 90mg BID or 60mg BID (regular)

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71
Q

ticagrelor needs to be used with caution if the patient also has what 2 conditions?

A

astham, bradycardia

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72
Q

what is the MOA of presugrel?

A

irreversible thienpyrodine inhibits ADP-mediated platelet activation at the P2Y12 receptor

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73
Q

use of prasugrel is c/i in what situations?

A

patinet has hx of stroke/transient ischemic attacks

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74
Q

what are the loading and regular doses for prasugrel?

A

loading: 60mg
regular: 10mg daily

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75
Q

which anticoagulants should be used for STEMI PCI?

A

enoxaparin, UFH, or bivalirudin

76
Q

which anticoagulants should be used for STEMI fibrinolysis?

A

enoxaparin or UFH

77
Q

which anticoagulants should be used for NSTEMI?

A

fondaparinux or UFH

78
Q

t/f an anticoagulant should be given to all ACS patients in addition to antiplatelet therapy regardless of treatment strategy

A

t

79
Q

why are anticoagulants given for ACS procedures?

A

reduces ischemic and thrombotic complications for STEMI patienst undergoing PCI

80
Q

MOA of UFH

A

indirect thrombin inhibitor on fibrin bound clots

81
Q

what are some disadvantages of UFH?

A
  1. variable ac response
  2. poorly bioavailable
  3. protein bound
  4. risk for HIT
82
Q

what are 2 advantages of UFH?

A

has a short half-life and not rebally cleared so can be used in renal impairment

83
Q

enoxaparin has balanced ___ and ___ activity

A

anti-factor Xa and anti iia activity

84
Q

which has a longer half life, UFH or enoxaparin?

A

enoxaparin

85
Q

does enoxaparin require anti-Xa monitoring?

A

no

86
Q

does enoxaparin require renal dosing adjustment?

A

yes

87
Q

for UA/NSTEMI, fondaparinux was found to be as effective as ____ with a reduced rate of major bleeding

A

enoxaparin

88
Q

what is the typical dose of fondaparinux?

A

2.5mg SC daily

89
Q

does fondaparinux need to be renally dose adjusted?

A

yes

90
Q

MOA of bivalrudin

A

direct thrombin inhibitor

91
Q

what is the typical dosing of bivalrudin for PCI?

A

IV bolus with infusion that is typically continued until the end of PCI

92
Q

Can bivalrudin be goven to a patient with hx or suspected present HIT undergoing PCI?

A

yes

93
Q

bivalrudin is not recommended if patient will under go ____

A

fibroloysis

94
Q

what fibrinolytic agents are available for STEMI?

A
  1. tenecteplase (TNK)
  2. alteplase (tPA)
  3. reteplase and streptokinase are no longer available in Canada
95
Q

___ specific fibrinolytoc agentsshowed lower mortality rates? Give examples of this type of agent

A

fibrin specific (tenecteplase, reteplase and accelerated alteplase infusion)

96
Q

mortality is signficantly decreased if lytic therapy is given within ___hours of symptom onset, with the greatest benefit of its within the first ___hrs

A

12; 2-3

97
Q

which lytic agent has a significantly higher 30 day survival rate in patients treated at >4 hours of symptom onset?

A

tenecteplase (TNK)

98
Q

list 4 complications of fibrinolysis therapy

A
  1. lack of initial reperfusion in ~20% of patients
  2. 5-8% of patients may have re-occlusion
  3. contraindications
  4. complications
99
Q

what are the absolute contraindications for fibrinolytic therapy?

A
  1. prior hemorrhagic stroke
  2. ischemic stroke in the last 3 months (unless in the last 4 hrs)
  3. intracranial neoplasm or arteriovenous malformation
  4. active internal bleeding
  5. aortic dissection
  6. considerable facial trauma or closed head trauma in past 3 months
  7. intracranial or intra-spinal surgery in last 2 months
  8. severe uncontrolled HTN that is unresponsive to emergency therapy
100
Q

what are the relative contraindications for fibrinolysis?

A
  1. BP>180/110 or poorly controlled HTN
  2. ischemic stroke in last 3 months
  3. major surgery <3 weeks before
  4. traumatic or prolonged CPR over 10 min
  5. internal bleeding in last 2-4 weeks
  6. active peptic ulcer
  7. non-compressible vascualr puncture
  8. pregnancy
  9. known intracranial pathology (dementia)
  10. oral anticoagulant therapy (as INR increases, so does bleeding risk)
101
Q

what is fibrinolysis?

A

rapid, non-selective thrombi lysis (not specific to coronary thrombus)

102
Q

fibrinolysis converts ___ to ____. What is the function of this newly formed agent?

A

plasminogen to plasmin. Plasmin the lyses the fibrin clot, resulting in fibrin degredation products

103
Q

in fibrinolysis, when fribringen is depleted, ___are degraded, which inhibits further clotting

A

clotting factors (I, II, V, and VIII)

104
Q

what is the brand name for alteplase (tPA)?

A

activase

105
Q

what is the MOA of alteplase (tPA)?

A

initiates fibrinolysis by binding fibrin in the clot and converting plasminogen to plasmin which breaks up the clot

106
Q

what is the accelerated infusion dosing for alteplase (tPA)?

A

15mg IV bolus then 0.75mg/kg over 30 min (max 50mg) or 0.5mg/kg over 60 minutes (max 35mg)

107
Q

what is the half-life of alteplase?

A

3.5 minutes (very short, this is why the infusion is needed)

108
Q

compare the efficacy of alteplase to tenecteplase for treating STEMI

A

the have equivalent efficacy (according to lecture)

109
Q

what ADRs need to be monitored after treatment with fibrinolytic?

A
  1. signs of bleeding
  2. change is neurological status that may suggest intracranial bleeding
  3. hypotension
110
Q

which fibrinolytic was found to have lower rates of non cerebral major bleeding?

A

tenectrplase

111
Q

fibronolytics should resolve the ST elevation by greater than ___% within ___minutes

A

50; 90

112
Q

fibrinolytics should make the patient pain free after ____minutes

A

90

113
Q

compare tenecteplase to alteplase

A

It is the same as alteplase, but has 3 mutations that make it more fibrin specific and it has more resistance to plasminogen activator inhibitor-1, and it has a longer half-life

114
Q

t/f the dosing of tenecteplase is bolus weight-based dsoing

A

t

115
Q

what is the half-life of tenecteplase?

A

11-20 minutes (allows for a single bolus dose)

116
Q

In what situations should early invasive strategies be used for NSTEACS treatment?

A
  1. refractory angina
  2. hemodynamic or electrical instability
  3. high risk based on clinical findings
  4. GRACE score >140
  5. TIMI score 5-7
  6. complex or extensive coronary artery disease (multi-vessel disease)
117
Q

with early invasive treatment for NSTEACS, the goal is _____hrs to cardiac cath unless unstable

A

24-48

118
Q

when is ischemic guided treatment a good option for NSTEACS?

A
  1. if no troponin elevation
  2. if its the patient/physician preference
  3. if patient is not a good candidate for revascularization (ex: renal failure)
  4. TIMI 0-1
  5. GRACE <109
119
Q

what is the typical treatment regimen for acute NSTEACS management?

A
  1. ASA 160mg chewed stat, then ECASA 81mg daily
  2. A P2Y12 inhibitor (clopidogrel 300mg then 75mg or ticagrelor 180mg then 90mg)
  3. Nitroglycerin (SL typical dose, then IV infusion), hold if hypotensive
  4. anticoagulant (fondaparinux 2.5mg daily for 8 days, UFH for renal patients or c/i).
  5. B blocker (caution if decompensating HF)
  6. ACE-i
  7. high dose statin
120
Q

at Nova Scotia Health, what is the use of Eptifibatide?

A

treatment of high risk patients (NSTEACS) in combo with anticoagulation for those undergoing cardiac cath in 24-48hrs
Also used as an adjunct to PCI with anticoagulation for the prevention of acute cardiac ischemic comlications

121
Q

most studies of GP inhibitors had them combined with which adjunct anticoagulant?

A

UFH

122
Q

what is the MOA of IV GP inhibitors?

A

block the final common pathway of platelet aggregation

123
Q

list three GP inhibitors

A
  1. eptifibatide
  2. tirofiban
  3. abciximab (not available in Canada)
124
Q

what is a common ADR of GP inhibitors?

A

increased bleeding risk

125
Q

when does the CCS recommend GP inhibitors not be used?

A

for STEMI patients undergoing PCI

126
Q

where in the body is bleeding most common after DAPT?

A

GI tract

127
Q

what are 2 issues with giving prophylactic PPI for gastric protection in DAPT?

A
  1. CYP2C19 inhibition of clopidogrel increases risk for stent thrombosis
  2. decreased Mg absorption which can lead to muscle spasms/cramps which may lead patients to think their statin needs to be stopped
128
Q

In what patients should a prophylactic PPI be used for DAPT?

A

those at high risk for GI bleeding (ex: active ulcer or recent ulcer)

129
Q

what is the function of SGLT2 inhibitors in ACS?

A

secondary prevention

130
Q

what were the findings of the EMPA-REG trial?

A

empagliflozin had NNT of 63/3.1 years for decreasing post ACS cardiovascular risk. It did cause genital infections

131
Q

what were the finsings of the CANVAS trial?

A

Canagliflozin NNT 62 / 3.6 years for decreased cardiovascualr event risk. Did have limb amputations

132
Q

what were the results of the DECARE-TIMI trial?

A

dapagliflozin had no change on cardiovascular risk compared to placebo

133
Q

what are some of the findings about colchicine for secondary prevention after ACS?

A

may decrease the risk slightly (they dont know why), but can have some odd side effects like increased nausea, non-fatal pneumonia (hospitalization), higher rate of all cause mortality (COPS trial)

134
Q

B blocker treatment after an ACS is lifelong if the EF is

A

40

135
Q

if a patient has an EF 40+%, how long is B blocker treatment for secondary ACS prevention?

A

1-3 years

136
Q

ACE-i therapy is indefinite for patients with what conditions?

A

EF <40%, DM, CKD

137
Q

when is an aldosterone antagonist used for secondary ACS prevention?

A

if patient has an EF <40% and already taking B blocker & ACE-i and its not enough to lower BP

138
Q

what needs to be monitored for aldosterone antagonists?

A

SCr and K (combo with ACE will increase the K)

139
Q

what is the MOA of aldosterone antagonists

A

inhibit the function of aldosterone which are: vascualr and myocardial fibrosis, endothelial dysfunction, HTN, sodium retention, K/Mg loss, arrhythmias

140
Q

how long is statin therapy after an ACS.?

A

life long

141
Q

what is the goal LDL after an ACS?

A

<1.8mmol/L

142
Q

when a plaque ruptures, the thrombogenix parts are exposed and this promotes platelet aggregation and adhesion through binding of _____ and synthesizes the release of ____

A

glycoprotein 1B to von willebrand factors; thromboxane A2, ADP and prothrombic substances

143
Q

ADP released by ruptured palques binds to ____ to promote changes in ____

A

P2y12 and P2y1; glycoprotein 2b23 surface receptors of platelets, increasing their affinity for fibrinogen

144
Q

platelets can cross link with each other by forming ___

A

fibrinogen bridges

145
Q

when a plaque is ruptured the _____ cascade is simultaneously activated due to exposure of blodd components to thrombogenic lipid core in endothelium

A

extrinsic coagulation cascade

146
Q

when a plaque ruptres, thrombin (factor 2a) is produced, what is its function?

A

converts fibrinogen to fibrin which stabilizes the clot and traps RBC. Also promotes platelet aggreation at injury site

147
Q

when clotting factors bind to the activated platelet surface, this promotes more ___ generation

A

thrombin

148
Q

t/f if you have more than one artery with a ruptured plaque, your prognosis is typically worse

A

t

149
Q

a thrombus with more ___ typically partially occludes vessels and presents as an NSTEMI

A

platelets

150
Q

a thrombus with more ___ and ___ typically fully occludes the artery and results in a STEMI

A

fibrin and RBC

151
Q

what is a missed or late presentation STEMI?

A

when patients do not go to the hospital right away bc they do not have typical symptoms

152
Q

when a patient presents with STEMI symptoms, a 12 lead ECG should be performed within ___minutes

A

10

153
Q

serial cardiac troponin should be obtained at presentation and at ___ and ___ hours after symptom onset

A

3 and 6

154
Q

t/f not all hospitals use the same assay for troponin, so the numbers for troponin will not always look the same

A

t

155
Q

for diagnosis of elevated tropinin, at least one reading needs to be above the __percentile of normal

A

99th

156
Q

over ___% of canadians live within 120 minutes of a PCI center

A

80

157
Q

reperfusion within __hrs of symptoms onset decreases mortality risk in STEMI patienst

A

12

158
Q

t/f STEMI care is best performed when there is an organized STEMI network

A

t

159
Q

when might GP inhibitors be appropriate for PCI?

A
  1. if patient threw up other antiplatelet

2. is there are residual thrombotic comlications after the PCI (large thromus burden, disection, no reflow)

160
Q

How can PCI cause a plaque fracture? what is the significance?

A

when the elastic components are stretched and the endothelium eerodes and results in a loss of nitric oxide. Plaque exposure causes vascualr recoil, platelet aggregation, thrombus formation, smooth muscle proliferation and synthesis of extreacellular matrix which can result in re-stenosis (why DAPTT is given)

161
Q

reperfusion arrhythmias are especially common after which type of reperfusion?

A

fibrinolysis

162
Q

the risk for hypotension caused by nitroglycerin needs to be considered especially of the patient has a risk for cardiogenic __

A

shock

163
Q

t/f B blockers have been shown to decrease myocardial ischemia, re-infarction and arrythmias

A

t

164
Q

PO B blockers are typically started within ___hrs in patients without signs of heart failure or increased risk of cardiogenic shock

A

24

165
Q

when are IV B blockers used?

A

if patient is tachycardic or hypertensive

166
Q

t/f B blockers also help with chest pain

A

t

167
Q

should ASA be taken with food? why or why not?

A

yes, to reduce GI side effects

168
Q

ASA has a short half-life, so why does it only need to be given UID?

A

because of irreversible inhibition

169
Q

prasugrel has not been shown to be beneficial unless the patient is undergoing ___

A

PCI

170
Q

why does ticagrelor have more ADR like SOB?

A

bc it inhibitos adenosine reuptake

171
Q

which has a faster and more consistent onset, clopidogrel or ticagrelor?

A

ticagrelor

172
Q

which anticoagulant is always used in dialysis patients?

A

UFH

173
Q

what were two other benefits of empagliflozin found in the EMPA-REG trial other than reduced CV events?

A

weight loss and lowered BP

174
Q

MOA of SGLT2-i

A

increase glucose excretion by preventing its reabsorption in the proximal tubule

175
Q

which B blockers should be avoided and why?

A

ones with sympathomimetic activity (acebutanol and pindolol) bc they may not permit sufficient reduction on HR

176
Q

abruptly stopping a B blocker can result in___

A

rebound tachycardia

177
Q

should patients stand or sit when taking their nitro spray?

A

sit bc it may cause dizziness

178
Q

can enoxaparin be used for anticoagulant for PCI and fibrinolysis?

A

yes

179
Q

t/f enoxaparin has shown reduced mortality risk and bleeding risk compared to UFH for PCI

A

t

180
Q

what is the “trigger” for going from primary to seconday prevention?

A

presence of atherosclerosis in the vascualr beds

181
Q

which test, CK or troponin is more accurate?

A

troponin bc it is specific to cardiac death and it is typically not present at baseline, unlike CK

182
Q

what are the half-lives of tropinin and CK?

A

CK: 2-3 days
Troponin: 1-2 weeks

183
Q

what is the name of the assay for cardiac troponin?

A

high sensitivity troponin assay

184
Q

compare metabolism of tirofiban and eptifitbatide

A

metabolism of tirofiban is negligable and the metabolism of eptifitabtide is made into inactive metabolites

185
Q

what is suggested by Q waves in leads I v2-V6?

A

MI

186
Q

Y

A

Y

PBL PY2 Fall (21 decks)

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