Angina and MI Flashcards

1
Q

What is angina?

A

Clinical syndrome of chest pain caused by an imbalance of myocardial blood flow supply and demand

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2
Q

What is variant angina?

A

Associated with eating, may present with SOB and is often due to coronary spasm

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3
Q

What is myocardial infarction?

A

Myocyte death caused by prolonged ischaemia

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4
Q

What is ischaemia caused by?

A

Oxygen supply/demand imbalance

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5
Q

Describe what happens in the majority of myocyte metabolism

A

Oxidative phosphorylation:
Uses fatty acids from breaking down triglycerides
Smaller amount of breakdown of glucose and lactate to pyruvate
Fatty acids and pyruvate oxidised to acetyl CoA, which is further oxidised in Krebs cycle leading to electrons which can be used to make ATP

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6
Q

What inhibits the breakdown of glucose and lactate to pyruvate?

A

Fatty acid oxidation

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7
Q

What happens to myocyte metabolism in the ischaemic myocardium?

A

There is a reduction in ATP formation by oxidative phosphorylation therefore a switch to glucose metabolism using glycolysis, leading to a build-up of lactate due to inability to oxidise pyruvate

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8
Q

What happens as a consequence of the ischaemic myocardium not being able to oxidise pyruvate?

A

There is a build-up of lactate leading to increase in H+ and lactate, and a decrease in pH leading to altered cell homeostasis

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9
Q

The amount of ATP produced by the Ca2+ pump is greater/less when pH is decreased

A

Greater

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10
Q

What is coronary autoregulation?

A

How the coronary arteries adjust to maintain a constant blood flow regardless of perfusion pressure

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11
Q

What mediates coronary autoregulation?

A

Myocyte
Vascular endothelial cell
Vascular smooth muscle cell

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12
Q

Describe the endothelial injury theory

A

Healthy endothelium is anti-inflammatory
Injury causes inflammatory response
Cytokines attract monocytes which cause increased endothelial permeability
Monocytes differentiate into macrophages which take take up oxidised LDL to become foam cells

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13
Q

How do T cells effect the injured endothelium

A

They secrete cytokines that induce smooth muscle cells to migrate from media to intima, and continue to proliferate to cause obstruction

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14
Q

Treatments for symptom relief that help the supply

A

Short acting nitrates
DHP calcium channel blockers
Long acting nitrates
Nicorandil

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15
Q

Treatments for symptom relief that help the demand

A

Beta blockers
Non-DHP calcium channel blockers
Ivabradine
Ranolazine

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16
Q

Examples of nitrates used for angina

A

Isosorbide mononitrate (or dinitrate), GTN

17
Q

How do nitrates work in angina?

A

Decrease preload and afterload
They act as NO donor to muscle converting GTP to cyclic GMP causing vasodilation

18
Q

Examples of beta blockers

A

Bisoprolol
Metoprolol
Carvedilol
Atenolol

19
Q

How do beta blockers work?

A

Reduce HR and contractility reducing demand
Block beta-adrenoreceptors in mycoytes and nodal tissues
Prevent adrenaline/noradrenaline binding, reducing calcium entry and myocyte contraction and activity
Reducing isotropy and chronotropy

20
Q

Examples of DHP CCBs

A

Amlodipine
Nifedipine

21
Q

How to CCBs work?

A

Cause smooth muscle relaxation and therefore vasodilation

22
Q

Which channels do CCBs work on?

A

LTCC

23
Q

Examples of non-DHP CCBs

A

Verapamil
Diltiazem

24
Q

Modes of action of nicorandil

A

Potassium channel activator, allowing potassium ions to exit the cell
Nitric oxide donor effect

25
Q

How does nicorandil shorten the action potential?

A

Reducing calcium entry into smooth muscle

26
Q

Mode of action of ivabradine

A

Funny current inhibitor (funny current only in the sinus node), reducing depolarisation, reducing HR without reducing inotropy or BP

27
Q

How does aspirin work?

A

Inhibits platelet activation and aggregation by inhibiting COX1, reducing thromboxane A2
Also increase prostaglandin I2