Pharmacology - CHD Flashcards

1
Q

Explain Coronary Blood Flow (CBF)

A

Venous blood returns to the right atrium, via the coronary sinus and anterior cardiac vein

Can also return to the heart chambers directly via thebesian veins

The right coronary artery then supplies blood to the SAN/AVN and the right hand

The left coronary artery supplies the left and right heart (85% of CBF)

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2
Q

What is the benefit of collateral vessels?

A

They are like B roads, so if there is ischemic damage (blockage in the main artery) then the blood can still flow around it

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3
Q

How is Coronary Blood Flow (CBF) regulated in the normal heart?

A

Autonomic NS has very little effect!!

Done by metobolic autoregulation, using potassium, adenosine and hypoxia

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4
Q

How does adenosine cause an increase in coronary blood flow (CBF)?

A

As heart rate/cardiac workload increases, more ATP is used up

The increase in AMP (from breakdown in ATP) stimulates an increase in adenosine

This stimulates A1 receptors (which decreases HR) and A2 receptors which increases cAMP levels…which causes vasodilation….and so increases CBF

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5
Q

How does Hypoxia and Potassium cause an increase in coronary blood flow (CBF)?

A

Hypoxia –> An increased workload causes less oxygen to be avaliable, and so less ATP in the coronary smooth muscle

This opens ATP-sensitive K+ channels, causing hypolarisation in the SM –> leading to vasodilation (increasing CBF)

Potassium –> An increased workload will increase the number of action potentials, which increases extracellular K+

This activates Na+K+-ATPase in the coronary SM, causing an increase in electronegativity –> causing hyperpolarisation…..and so more vasodilation and CBF

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6
Q

What are the 4 different types of Angina?

A

Myocardial Infarction (ACS) –> At rest

Unstable Angina (ACS) –> At rest, due to plaque rupture

Stable Angina –> On excertion/stress

Variant Angina –> At rest, caused by coronary vasospasms

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7
Q

How do you treat Stable Angina?

A

Reduce oxygen demand

Increase oxygen supply

Use lipid lowering drugs to prevent the progression of the atheromatous disease

First Line = BB (B1 selective) / CCB (dihydropyridines)

Second line = Organic nitrates/Ivabradine/Nicorandil/Ranolazine

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8
Q

How do Organic Nitrates work?

A

They are metabolised to release NO –> increasing levels of cGMP…which causes relaxation

Cause the systemic vasodilation of veins (decreases preload) and arteries (decrease afterload), which causes a decrease in cadiac oxygen demand

Also causes an increase in the dilation of collateral vessels, which increase oxygen supply

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9
Q

How do Nicorandil, Ivabradine and Ranolazine work?

A

Nicorandil –> Activates vascular ATP-sensitive K+ channels, and is also an NO donor

Ivabradine –> Inhibits the if pacemaker current in the SAN, which decreases HR

Ranolazine –> Inhibits late Na+ channels that are activated by ischaemia in cardiac myocytes

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10
Q

How do you treat Variant Stable?

A

Nitrate Vasodilator + CCB

BB are NOT effective

As main aim is to dilate coronary arteries

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11
Q

What are the 2 types of Unstable Angina?

A

NSTEMI –> Partial artery blockage

STEMI –> Complete artery blockage

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12
Q

What’s the difference between Pulmonary and Peripheral Oedema?

A

Pulmonary –> Left ventricular hypertrophy

Peripheral –> Congestive heart faliure (CHF)

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