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Coronary Heart Disease > ACS > Flashcards

ACS Flashcards

1
Q

What do all ACS result from?

A

an acute plaque rupture in wall of epicardial coronary artery

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2
Q

3 clinical subtypes of CAD

A

UA
NSTEMI
STEMI

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3
Q

NSTEMI (stand for)

A

non-ST segment elevation myocardial infarction

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4
Q

STEMI

A

ST segment elevation myocardial infarction

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5
Q

Which types are incomplete/transient?

A

UA

NSTEMI

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6
Q

Which types are complete/sustained?

A

STEMI

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7
Q

What is the difference between UA and NSTEMI?

A

difference in duration and severity of ischaemia and symptoms

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8
Q

What type is more severe?

A

STEMI

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9
Q

characteristics of UA

A
  • acceleration in severity/frequency of chest pain
  • new anginal pain
  • pain at rest
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10
Q

Necrosis in UA?

A

no

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11
Q

Necrosis in NSTEMI?

A

yes

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12
Q

Features of STEMI

A
  • abnormal cardiac rhythms
  • increased risk of sudden death
  • cell necrosis
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13
Q

When does necrosis occur in STEMI and NSTEMI?

A

within 20-40mins

significant death after 2-3hrs

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14
Q

2 phases in STEMI/NSTEMI

A
  1. ischaemia

2. infarction

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15
Q

What 3 changes can be seen on ECG?

A
  • ST changes
  • T wave inversion
  • pathological Q wave development
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16
Q

What causes an inverted T wave?

A

altered repolarisation

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17
Q

What is ST elevation a sign of?

A

myocardial injury

18
Q

What do abnormal Q waves result from?

A

absence of depolarisation current from dead tissue and presence of opposing currents from other areas in heart

19
Q

ECG changes in STEMI

A

ST elevation

pathological Q wave development

20
Q

ECG changes in UA/NSTEMI

A

ST depression
T wave inversion
(persistent in NSTEMI and transient in UA)

21
Q

4th diagnosis for ACS?

A

elevated troponin levels

22
Q

What is given for immediate management of ACS?

A 
aspirin 300mg
additional O2
GTN
diamorphine/morphine
beta blocker 4
23
Q

clinical management for STEMI

A

coronary revascularisation/reperfusion

24
Q

Open artery theroy

A

prompt and complete restoration of flow in occluded artery decreases infarct size, preserves LV function and improves survival rates

25
Q

2 types of coronary revascularisation

A
  • mechanical (PCI)

- pharmacological (thrombolytic/fibrinolytic therapy)

26
Q

2 treatments for UA and NSTEMI

A
  • initial conservative strategy

- early invasive strategy

27
Q

What is the initial conservative strategy?

A

antiplatelet and anticoagulant therapy (low risk patients)

28
Q

What is the early invasive strategy?

A

mechanical or surgical reperfusion (PCI/CABG)

29
Q

What are the 2 pathways for antithrombotic therapy?

A

prothrombotic and antithrombotic pathways

30
Q

What happens in the prothrombotic system?

A

blood clot formed

31
Q

What happens in the antithrombotic systam?

A

blood clot dissolved

32
Q

2 thrombolytic agents

A
  • streptokinase (SK)

- tissue type plasminogen activators (t-PAs)

33
Q

When is thrombolytic therapy used?

A

if PCI not possible within 120mins of STEMI diagnosis

34
Q

Side effects of thrombolytic therapy

A
  • haemorrhage
  • allergic reaction (SK)
  • hypotension
  • reperfusion induced arrhythmias
35
Q

antiplatelet agents

A

cyclooxygenase inhibitors (aspirin)
ADP receptor antagonists
GP2b/3a receptor antagonists

36
Q

What is factor IIa?

A

thrombin

37
Q

What does anticoagulant therapy inactivate?

A

IIa and/or Xa and 9a

38
Q

Drugs used in anticoagulant therapy?

A
  • unfractionated heparin (UFH)
  • LMW heparins
  • synthetic pentasaccharides
  • direct thrombin inhibitors
39
Q

What are the 2 classes of anticoagulants?

A
  1. indirect thrombin inhibitors

2. direct thrombin inhibitors

40
Q

3 types of indirect thrombin inhibitors

A
  • UF heparin
  • LMW heparins
  • fondaparinux
41
Q

1 direct thrombin inhibitor

A

bivalirudin

Coronary Heart Disease (14 decks)

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