MI and Ischaemic Heart Disease Flashcards

1
Q

What is chronic angina?

A

Demand led ischaemia of the heart muscle due to a fixed stenosis

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2
Q

What is the recommendation for patients who have an angina attack and have stable angina?

A

Stop ,sit and use GTN spray

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3
Q

When may angina commonly be felt?

A
  • after a meal

- in cold air

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4
Q

Where does pain for angina commonly radiate?

A
  • Jaw
  • Back
  • Epigastrium
  • Left (and right) arm
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5
Q

What type of pain is felt with angina?

A

Heavy crushing pain with tightness

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6
Q

What are the two types of acute MI?

A
  1. STEMI

2. NON-STEMI

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7
Q

Why does acute coronary syndrome occur?

A

Development of an atheromatous plaque that develops a thrombosis and ruptures

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8
Q

Which steps lead to thrombosis occurring?

A
  • Normal
  • Fatty streak
  • Atherosclerotic plaque
  • Fibrous plaque
  • Rupture/ thrombosis
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9
Q

In what ways is chronic stable angina different to an acute coronary syndrome such as unstable angina?

A
  • it has a fixed stenosis (not complete occlusion)
  • Demand led ischaemia (not supply led)
  • Predictable
  • Safe
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10
Q

What are the three sub-stages of thrombosis formation?

A
  1. Initiation
  2. Adhesion
  3. Activation
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11
Q

Describe the imitation stage of thrombosis formation

A

There is vascular damage exposing the sub- endothelium, collagen and von Willebrand factor

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12
Q

Describe the adhesion stage of thrombosis formation

A

Platelets recruit to the area and bind to the exposed collagen and von Willebrand factor forming a monolayer

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13
Q

Describe the activation stage of thrombosis formation

A
  • platelets become activated after adhesion and change shape from discs to star-like shapes
  • Platelets release ADP and thromboxane A2 (generated by cyclooxyrgenase)
  • ADP binds to receptors on circulating platelets allowing more activation to occur
  • Activated platelets express adhesion sites for leukocytes (P-selectin and CD40 ligand)
  • These processes contribute to the platelet cascade which causes acceleration of platelets activation and coagulation
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14
Q

What is the consequence of intraluminal coagulation ?

A

Vascular blockage

Hence MI, stroke and death are all possible

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15
Q

What are the key symptoms of MI?

A
  • Severe crushing (10/10) pain not relived by GTN and lasting a long time
  • Pain occurs at rest
  • Pain radiated to jaw, left (and right) arm, back and epigastric region
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16
Q

For an MI, where will the changes be seen on an ECG?

A
  • ST elevation
  • T wave inversion
  • Q waves
17
Q

How is a STEMI seen on an ECG?

A
  • > /= 1mm ST elevation in 2 adjacent limb leads
  • > /= 2mm ST elevation in at least 2 continuous precordial leads
  • New onset bundle branch block
18
Q

How does the ECG change after an MI?

A
  1. Initially an ST elevation is present (a few hours)
  2. Q wave formation and T wave inversion follow (within a day)
  3. Finally, Q waves are present with or without T waves
19
Q

In an inferior MI, which limb leads will be affected?

A

II, III, aVF

20
Q

In an anterior MI, which limb lead can be affected?

A

V1-6

21
Q

In an anteroseptal MI, which limb leads are affected?

A

V1-4

22
Q

In an anterolateral MI, which limb leads are affected?

A

I, aVL, V1-6

23
Q

Which two urine tests can help in the diagnosis of MI?

A
  1. Creatinine Kinase

2. Troponin C

24
Q

At what time will Creatinine kinase levels peak in the urine after MI and what does this signify?

A

Within 24 hours
Creatinine kinase found in muscle and brain cells
Suggests muscle damage

25
Q

What does the presence of troponin C in urine suggest?

A

Highly specific for cardiac muscle

It is a good indicator for myocardial necrosis

26
Q

How is a STEMI immediately treated?

A

Aspirin - 300 mg

Clopidogrel- 300 mg

27
Q

What is clopidogrel?

A

AN inhibitor of ADP binding sites (P2Y12 receptor) which prevents activation of Glycoprotein IIb/IIIa (fibrinogen receptors) on platelets

28
Q

How does aspirin work?

A

Aspirin prevent cyclooxyrgenase (COX-1) activation in platelets
This prevents production of thromboxane A2
(it also blocks COX in endothelial cells blocking production of anti-thrombotic prostaglandin I2 is inhibited- this is not useful)

29
Q

What is thrombolysis?

A

A way of unblocking arteries by breaking down clots using thrombolytic drugs such as streptokinase

30
Q

When should thrombolysis be administered?

A
  1. Chest pain is suggestive of acute MI (more than 20 minutes and less than 12 hours)
  2. ECG changes - acute ST elevation, new LBBB
  3. No contraindications
    It is NOT administered if PCI will be available