MI and Ischaemic Heart Disease Flashcards

(30 cards)

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?

20
Q

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

21
Q

In an anteroseptal MI, which limb leads are affected?

22
Q

In an anterolateral MI, which limb leads are affected?

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
What does the presence of troponin C in urine suggest?
Highly specific for cardiac muscle | It is a good indicator for myocardial necrosis
26
How is a STEMI immediately treated?
Aspirin - 300 mg | Clopidogrel- 300 mg
27
What is clopidogrel?
AN inhibitor of ADP binding sites (P2Y12 receptor) which prevents activation of Glycoprotein IIb/IIIa (fibrinogen receptors) on platelets
28
How does aspirin work?
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
What is thrombolysis?
A way of unblocking arteries by breaking down clots using thrombolytic drugs such as streptokinase
30
When should thrombolysis be administered?
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