1. ACS Flashcards

1
Q

When a coronary artery gets occluded, all of the myocardium _______ to the blockage becomes ________.

A
  • distal

- ischemic

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2
Q

Why does a fibrous cap form over the plaque?

A

To prevent blood cells and proteins from interacting with the plaque.

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3
Q

Activated platelets actively circulate throughout body. (T/F)

A

False: inactivated platelets

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4
Q

Why do platelets clot on plaques?

A

They “think” the vessel is/ is going to bleed.

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5
Q

In unstable angina, to what degree is the vessel occluded by the thrombus?

A

incomplete occlusion

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6
Q

A sign of unstable angina is that pain occurs ________.

A

at rest

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7
Q

What is the difference between unstable angina and NSTEMI?

A

NSTEMI creates myocardial necrosis which is indicated by elevated troponin levels

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8
Q

What labs are used to diagnose NSTEMI?

A
  • cardiac troponin T or I assay

- creatine kinase myocardial band

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9
Q

Acute myocardial infarction is associated with EKG ___________ elevation.

A

ST segment

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10
Q

A _______ is caused by total coronary occlusion which causes __________.

A
  • STEMI

- severe necrosis

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11
Q

necrosis spanning the whole muscle

A

trans-mural

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12
Q

MI severity is proportional to what?

A

troponin levels

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13
Q

Why is the ST segment elevated in a severe MI?

A

The ion channels are not functioning properly enough to make a normal action potential. Could be a result of insufficient ATP.

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14
Q

Describe the progression of myocardial tissue necrosis.

A
  • vessel occlusion
  • insufficient myocardial profusion
  • tissue necrosis
  • arrhythmias develop
  • ventricular fibrillation
  • heart stops
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15
Q

Describe stable angina pain.

A
  • deep, poorly localized chest or arm discomfort

- rarely described as pain: often described as strangling or suffocating feeling

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16
Q

Stable angina pain is associated with what behaviors?

A
  • physical exertion

- emotional stress

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17
Q

What measures should be taken to relieve stable angina pain?

A
  • 5 – 15 minutes of rest

- sublingual nitroglycerin

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18
Q

In a patient with stable angina, worsening or more frequent pain is associated with what?

A

more extensive ischemia and could lead to MI

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19
Q

Unstable angina is defined as having at least one of these 3 features:

A
  • occurs at rest usually lasting more than 20 minutes (if not interrupted by NG
  • definite pain that has not occurred previously
  • occurs with an advancing pattern
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20
Q

What pathophysiological processes are responsible for unstable angina?

A
  • plaque rupture with non-occlusive thrombus
  • coronary vasoconstriction from vasospasm
  • inflammation and/or infection
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21
Q

What are the 3 treatment objectives for UA/NSTEMI?

A
  • stabilize the acute coronary lesion
  • treatment of residual ischemia
  • long-term secondary prevention
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22
Q

What are the anti-thrombotic therapies for UA/NSTEMI?

A
  • ASA
  • heparin
  • glycoprotein IIb/IIIa inhibitors
  • ADP antagonists
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23
Q

Anti-thrombotic therapies reverse existing clots. (T/F)

A

False: they prevent further thrombosis and allow endogenous fibrinolysis to dissolve the thrombus

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24
Q

Anti-thrombotics are continued long-term for what reason?

A

reduce the risk of developing future events

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25
What are the anti-ischemic therapies for UA/NSTEMI?
- beta-blockers - nitrates - calcium antagonists
26
How do anti-ischemic therapies treat UA/NSTEMI?
reducing oxygen demand and improving blood flow
27
After stabilizing the acute event, what atherosclerotic risk factors should be addressed?
- hypercholesterolemia - HTN - smoking
28
Why are ACEIs used in UA/NSTEMI?
- reduce ventricular remodeling after infarction | - prevents further muscle damage
29
What dose of ASA should be given during CV event?
162 - 325mg chewed
30
What is the dose range of typical long-term ASA therapy?
75 - 360 mg/day
31
What are CIs for ASA therapy?
- aspirin allergy - active bleeding - known platelet disorder
32
What is the MOA of ADP antagonists?
- inhibit platelet aggregation - increases bleeding time - reduces blood viscosity by inhibiting ADP (activation) action on platelet receptors
33
What are the ADP antagonist agents?
- Clopidogrel (Plavix) - Prasugrel - Ticagrelor
34
In what cases is clopidogrel a preferred agent?
ASA allergy
35
What is the MOA of IIb/IIIa inhibitors
- bind to platelet glycoprotein IIb/IIIa (receptor proteins) | - block the final common pathway of platelet aggregation
36
ASA is considered a relative weak anti-platelet agent. (T/F)
True
37
GP IIb/IIIa inhibitors block platelet aggregation from which stimuli?
All of them: - thromboxane A2 - ADP - thrombin - collagen - serotonin
38
What are the GP IIb/IIIa inhibitor agents?
- Abciximab - Tirofiban - Eptifibatide
39
By what route are GP IIb/IIIa inhibitor agents administered?
IV
40
Define hemostasis
physiological system that preserves integrity of the circulation
41
During normal conditions, what does hemostasis promote?
blood fluidity
42
During loss of blood, what does hemostasis promote?
designed to clot very rapidly at the specific site of injury
43
After healing, what does hemostasis promote?
restoring blood flow and perfusion to tissues supplied by the damaged vessel
44
What are the 3 major components of the hemostatic system?
- vessel wall - platelets - plasma proteins
45
What portion of the vessel wall plays a role in hemostasis?
endothelial cells
46
Which plasma proteins play a role in hemostasis?
- coagulant proteins - anticoagulant proteins - fibrinolytic proteins
47
What are the 4 phases of hemostasis?
1) vascular phase 2) platelet phase 3) coagulation phase 4) fibrinolytic phase
48
What is the vascular phase?
- the initial trigger to activate hemostatic processes | - stimulate constriction
49
When will platelets adhere to the vessel wall?
when the subendothelial collagen and von Willebrand factor is exposed
50
What protein binds to the GP IIb/IIIa to link cross-link 2 platelets?
- fibrinogen | - vWF
51
Where is thromboxane A2 produced?
in the platelets
52
What is the role of TXA2?
- induces release of granule contents - increases expression of GP IIb/IIIa - stimulates platelet activation
53
The clotting cascade is activated ultimately resulting in what?
the formation of a fibrin clot
54
The coagulation phase occurs simultaneously with platelet activation. (T/F)
True
55
What are the 2 coagulation pathways?
intrinsic and extrinsic
56
Which coagulation pathway is not critical in the body?
intrinsic
57
Deficiency of factor ___ causes hemophilia A.
VIII
58
Deficiency of factor ___ causes hemophilia B.
IX
59
The extrinsic pathway is _____ _______ activated.
tissue factor
60
Which coagulation pathway is the primary physiological pathway?
extrinsic
61
What exposes blood to TF?
vascular damage
62
TF binds to _____ forming a complex that produces more ____.
VIIa | VIIa
63
VIIa+TF activates factor __ and activates factor __ from the intrinsic pathway
- X | - IX
64
The common pathway is initiated by factor Xa converting _______ to ________.
prothrombin | thrombin
65
What is considered the most critical protease of the coagulation system?
thrombin
66
Factor ___ is a cofactor required in converting prothrombin to thrombin.
Va
67
Thrombin converts ______ to ______.
soluble plasma protein fibrinogen to insoluble fibrin
68
The endothelium produces ______ and ________ to prevent clotting.
- PGI2 (prostacyclin) | - nitric oxide
69
What is the major plasma protease inhibitor?
Antithrombin III
70
What protein degrades factors Va and VIIIa?
Protein C
71
Protein C degrades what?
factors Va and VIIIa
72
What is the role of protein S?
cofactor that accelerates protease action of protein C
73
What is the fibrinolytic phase?
endogenous system activated when thrombin escapes the anticoagulant systems
74
What is the purpose of the fibrinolytic phase?
dispose of intravascular fibrin
75
What is the key protease of the fibrinolytic system?
plasmin
76
What is plasmin?
protease that digests fibrin into fibrin degradation products
77
What are the plasminogen activators?
- tissue-type plasminogen activator (t-PA) | - urokinase-type plasminogen activator (u-PA)
78
What directly binds plasmin to inhibit its activity?
Alpha 2-antiplasmin