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951 Block 3 > 1. ACS > Flashcards

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
Q

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

A
  • beta-blockers
  • nitrates
  • calcium antagonists
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26
Q

How do anti-ischemic therapies treat UA/NSTEMI?

A

reducing oxygen demand and improving blood flow

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27
Q

After stabilizing the acute event, what atherosclerotic risk factors should be addressed?

A
  • hypercholesterolemia
  • HTN
  • smoking
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28
Q

Why are ACEIs used in UA/NSTEMI?

A
  • reduce ventricular remodeling after infarction

- prevents further muscle damage

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29
Q

What dose of ASA should be given during CV event?

A

162 - 325mg chewed

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30
Q

What is the dose range of typical long-term ASA therapy?

A

75 - 360 mg/day

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31
Q

What are CIs for ASA therapy?

A
  • aspirin allergy
  • active bleeding
  • known platelet disorder
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32
Q

What is the MOA of ADP antagonists?

A
  • inhibit platelet aggregation
  • increases bleeding time
  • reduces blood viscosity by inhibiting ADP (activation) action on platelet receptors
33
Q

What are the ADP antagonist agents?

A
  • Clopidogrel (Plavix)
  • Prasugrel
  • Ticagrelor
34
Q

In what cases is clopidogrel a preferred agent?

A

ASA allergy

35
Q

What is the MOA of IIb/IIIa inhibitors

A
  • bind to platelet glycoprotein IIb/IIIa (receptor proteins)

- block the final common pathway of platelet aggregation

36
Q

ASA is considered a relative weak anti-platelet agent. (T/F)

A

True

37
Q

GP IIb/IIIa inhibitors block platelet aggregation from which stimuli?

A

All of them:

  • thromboxane A2
  • ADP
  • thrombin
  • collagen
  • serotonin
38
Q

What are the GP IIb/IIIa inhibitor agents?

A
  • Abciximab
  • Tirofiban
  • Eptifibatide
39
Q

By what route are GP IIb/IIIa inhibitor agents administered?

A

IV

40
Q

Define hemostasis

A

physiological system that preserves integrity of the circulation

41
Q

During normal conditions, what does hemostasis promote?

A

blood fluidity

42
Q

During loss of blood, what does hemostasis promote?

A

designed to clot very rapidly at the specific site of injury

43
Q

After healing, what does hemostasis promote?

A

restoring blood flow and perfusion to tissues supplied by the damaged vessel

44
Q

What are the 3 major components of the hemostatic system?

A
  • vessel wall
  • platelets
  • plasma proteins
45
Q

What portion of the vessel wall plays a role in hemostasis?

A

endothelial cells

46
Q

Which plasma proteins play a role in hemostasis?

A
  • coagulant proteins
  • anticoagulant proteins
  • fibrinolytic proteins
47
Q

What are the 4 phases of hemostasis?

A

1) vascular phase
2) platelet phase
3) coagulation phase
4) fibrinolytic phase

48
Q

What is the vascular phase?

A
  • the initial trigger to activate hemostatic processes

- stimulate constriction

49
Q

When will platelets adhere to the vessel wall?

A

when the subendothelial collagen and von Willebrand factor is exposed

50
Q

What protein binds to the GP IIb/IIIa to link cross-link 2 platelets?

A
  • fibrinogen

- vWF

51
Q

Where is thromboxane A2 produced?

A

in the platelets

52
Q

What is the role of TXA2?

A
  • induces release of granule contents
  • increases expression of GP IIb/IIIa
  • stimulates platelet activation
53
Q

The clotting cascade is activated ultimately resulting in what?

A

the formation of a fibrin clot

54
Q

The coagulation phase occurs simultaneously with platelet activation. (T/F)

A

True

55
Q

What are the 2 coagulation pathways?

A

intrinsic and extrinsic

56
Q

Which coagulation pathway is not critical in the body?

A

intrinsic

57
Q

Deficiency of factor ___ causes hemophilia A.

A

VIII

58
Q

Deficiency of factor ___ causes hemophilia B.

A

IX

59
Q

The extrinsic pathway is _____ _______ activated.

A

tissue factor

60
Q

Which coagulation pathway is the primary physiological pathway?

A

extrinsic

61
Q

What exposes blood to TF?

A

vascular damage

62
Q

TF binds to _____ forming a complex that produces more ____.

A

VIIa

VIIa

63
Q

VIIa+TF activates factor __ and activates factor __ from the intrinsic pathway

A
  • X

- IX

64
Q

The common pathway is initiated by factor Xa converting _______ to ________.

A

prothrombin

thrombin

65
Q

What is considered the most critical protease of the coagulation system?

A

thrombin

66
Q

Factor ___ is a cofactor required in converting prothrombin to thrombin.

A

Va

67
Q

Thrombin converts ______ to ______.

A

soluble plasma protein fibrinogen to insoluble fibrin

68
Q

The endothelium produces ______ and ________ to prevent clotting.

A
  • PGI2 (prostacyclin)

- nitric oxide

69
Q

What is the major plasma protease inhibitor?

A

Antithrombin III

70
Q

What protein degrades factors Va and VIIIa?

A

Protein C

71
Q

Protein C degrades what?

A

factors Va and VIIIa

72
Q

What is the role of protein S?

A

cofactor that accelerates protease action of protein C

73
Q

What is the fibrinolytic phase?

A

endogenous system activated when thrombin escapes the anticoagulant systems

74
Q

What is the purpose of the fibrinolytic phase?

A

dispose of intravascular fibrin

75
Q

What is the key protease of the fibrinolytic system?

A

plasmin

76
Q

What is plasmin?

A

protease that digests fibrin into fibrin degradation products

77
Q

What are the plasminogen activators?

A
  • tissue-type plasminogen activator (t-PA)

- urokinase-type plasminogen activator (u-PA)

78
Q

What directly binds plasmin to inhibit its activity?

A

Alpha 2-antiplasmin

951 Block 3 (10 decks)

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