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Supporting Life > Pharmacology of Angina > Flashcards

Pharmacology of Angina Flashcards

1
Q

What is the full name of angina?

A

Angina pectoris

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2
Q

What is the name of the process of cholesterol rich plaques building up in vessels?

What is the risk of this condition in the:

A) coronary vessels
B) renal arteries
C) carotid arteries

A

Atherosclerosis

A) MI
B) chronic kidney disease
C) stroke

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3
Q

What are the 2 parts of an atherosclerotic plaque?

A

Fibrous cap in tunica intima

Atheroma (fatty rich soft core of extracellular lipid)

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4
Q

What happens with time to the atheroma?

A

It will calcify

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5
Q

Where do plaques usually form with respect to the coronary arteries and surrounding structures?

A

Within 6cm of the aorta

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6
Q

What are 2 types of plaques and are there and what are the qualities of each?

Which are more likely to turn into which conditions?

A

Vulnerable plaque - stable angina
= think fibrous cap
= large atheroma

Non-vulnerable plaque - unstable angina, STEMI, NSTEMI (basically ACS)
= thick fibrous cap
= small atheroma

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7
Q

Can the two types of plaques interconvert?

A

Yes

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8
Q

Name 5 times of angina.

A

1) angina of effort (stable)
2) mixed (variable threshold) angina
3) Vasospastic (prinzmetal’s) angina
4) microvascular (Syndrome x)
5) unstable

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9
Q

Explain stable angina (of effort).

A

Occurs with exertion/emotion
Stops with rest or GTN
Results from increase oxygen demand but lack of ability to vasodilate and increase blood flow due to fixed stenosis and a decreased flow reserve capacity

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10
Q

What peptide does hypoxia cardiac cells release and what effect does this have on the body?

Via what channels?

A

They release bradykinin, activates Trpv1 channels on sensory nerves to cause pain!

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11
Q

How does pain help with angina?

A

Pain causes substance P release from sensory nerve endings, which include to NK1 Receptors on the vessel walls to cause NO release, therefore substance P is a potent vasodilator which helps to combat angina

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12
Q

Explain vasospastic (primzmetal’s) angina.

A

No vessel stenosis
Occurs due to vasospasm of the coronary arteries
Happens at night
Rarer

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13
Q

Explain mixed (variable threshold) angina.

A

A mixture of stable angina of effort and vasospasti (prinzmetal’s)
Unpredictable
Happens at varying levels or exercise
A mix of stenosis and vasospasm

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14
Q

Explain microvascular (syndrome x) angina.

A

Common in females (hence name)
No stenosis BUT chest pain and positive exercise test
Microvasculature (arterioles) affected NOT macrovasculature (arteries)

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15
Q

Explain unstable angina.

A

Formation of a non-occlusive thrombus, caused by plaque rupture and thrombus formation.
It an ACS

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16
Q

What is the main aim of drug treatment for angina, and why is this the case?

A

The main aim is to decrease cardiac oxygen demand and increase the oxygen supply to the ischaemic zone by decreasing heart rate, as vasodilation is NOT an option.

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17
Q

How do the following drugs work and what do they hope to achieve?

1) b-blockers
2) ACE inhibitors
3) aspirin
4) statins

A

1) decrease inotropy and chronotropy
2) decrease BP and pressures
3) anti-platelet
4) decrease cholesterol

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18
Q

What is the NICE pathway for treatment of stable angina?

A

1) short acting nitrate for immediate relief
2) beta-blocker AND non-vascular selective CCB
3) beta-blocker and VASCULAR selective CCB
4) beta-blocker and vascular selective CCB AND one of the following:
- long acting nitrate
- ivabradine
- nicorandil (potassium channel activator)
- ranolazine (anti-anginal)

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19
Q

How do nitrates work vascularly?

What effect does this have on the heart?

A

They venodilate

This decreases cvp which decreases pressures going into the heart, which decreases preload and cardiac oxygen demand

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20
Q

In what X3 ways does NO cause smooth muscle relaxation?

A

Desensitises muscle fibres to calcium
Opens calcium pumps
Opens potassium channels to decrease membrane polarisation

21
Q

What are the main natural endogenous vasoconstrictors?

A

Adrenaline (not for coronary arteries)
Noradrenaline
Angiotensin 2
Vasopressin (ADH)

22
Q

What does angiotensin 1 and 2 do?

A

1 is purely a precursor for 2, it has no biological effect

2 is a vasoconstrictor has a myriad of functions with the aim of vasoconstriction. It itself vasoconstricts.

23
Q

Which receptor adrenergic receptor is responsible for vasoconstriction?

Which GPCR is this coupled to?

A

Alpha 1

Gq

24
Q

What is the Gq pathway?

A

Increases PLC activity

Which increases ip3 and DAG levels

25
Q

What does ip3 do intracellularly?

A

Causes calcium release from the SR

26
Q

What does DAG do intracellularly?

A

Opens receptor gated sodium and calcium channels

27
Q

What is the main mechanism of calcium influx in vasoconstriction?

A

Ip3 and DAG cause membrane depolarisation, which in turn opens VOLTAGE gated calcium channels (NOT RECEPTOR gated ones like DAG) which cause the majority of calcium influx and therefore depolarisation

28
Q

What is the alpha 2 associated GPCR and what is its pathway?

A

Gi

It works via inhibition of andenylate cyclase, stopping it turn ATP into cyclic AMP (CAMP)

29
Q

What is the beta 1 associated GPCR and what is its pathway?

A

Gs

It works via activation of andenylate cyclase, increasing its yield of ATP into cyclic AMP (CAMP)

30
Q

What is the main method of natural vasodilation?

A

Endothelial cells releasing nitric oxide (NO)

31
Q

How does NO work to cause vasodilation?

A

NO activated gaunylate cyclase which causes GTP —> cyclic GMP (CGMP). CGMP then pumps calcium out of cells and into the SR whilst also opening potassium channels to hyperpolarise the cell.

32
Q

Which enzyme group breaks down the second messenger molecules CAMP and CGMP?

A

PDE (phosphodiesterases)

33
Q

Other than GTN, name another organic nitrate used to treat or recent angina?

How does this differ to GTN?

What are it’s flaws and how is this overcome?

A

Isosorbide dinitrate

It is a longer acting and is prophylactic as opposed to acute treatment

Tolerance develops

This can be avoided via 8 hour drug free periods at night

34
Q

How do organic nitrates work to treat angina?

A

They are NO donors, which therefore causes vasodilation (of veins more than arteries)

35
Q

Why do organic nitrates vasodilation veins more than arteries?

A

Because the reactive oxygen species they produce in breakdown cause endothelin 1 release from endothelial cells which increase the response that vasoconstrictors have on the vessels. This almost counteracts the nitrate effects, giving GTN and others selective vein effects.

36
Q

Which enzyme breaks down GTN?

Which enzyme group breaks down longer acting lower potency organic nitrates?

A

MtALDH2

Cytp450

37
Q

Where are beta 1 receptors mostly found?

What is the effect of their stimulation?

A

Mostly found in the heart

They increase inotropy and chronotropy

38
Q

Where are beta 2 receptors mostly found?

What is the effect of their stimulation?

A

Mainly found in smooth muscle (e.g. airways and blood vessels)

They cause relaxation of the smooth muscle and vasodilate

39
Q

How do beta blockers work to treat angina?

A

They block the beta receptors which decreases inotropy and chronotropy, which decreases the oxygen demand placed on the heart and allows increased coronary flow within diastole

They also cause renin release which decreases BP and therefore decreases afterload, overall decreasing the oxygen demand placed on the heart

40
Q

Which type of angina would you NOT give beta blockers for?

A

Vasospastic (prinzmetal’s) as you DO NOT want to remove the vasodialting ability of the vessels by blocking beta 2 receptor activity

41
Q

What are the 2 types of calcium channel blocker effects?

A

1) vasodilation

2) negative inotropy and chronotropy

42
Q

Which of these beta blockers are selective for what type of beta receptor?

1) bisoprolol
2) butaxamine
3) labetalol
4) metoprolol
5) atenolol

A

1) B1
2) B2
3) Non-selective
4) B1
5) B1

43
Q

Name three drugs or drug groups of calcium channel blockers in order of best for vasodilating to worst?

How does this change for negative inotropic and chronotropic effects?

A

Dihydropyridines (DHP) e.g. amplodipine/nifedipine (all have ‘pine’ ending)

Diltiazem

Verapamil

This list reverses

44
Q

Which drug or group is therefore a vascular selective CCB?

A

Amlodipine or other DHP’s

45
Q

How does nicorandil work?

A

It is a potassium channel activator therefore works the same as natural NO mediated vasodilation (as it opens the same channels)

46
Q

What does ivabridine do and how?

Describe the mechanism of action.

A

It blocks the funny current (If) by entering the open channel and gets trapped when channel shuts

This decreases heart rate allowing more time for diastolic myocardial perfusion

47
Q

How do statins work?

A

They block HMG-CoA enzyme which is the rate limiting enzyme in cholesterol synthesis in the liver

The liver therefore takes LDL fro, the vasculature to make up from this, lowering the amount of free LDL in the vessels

48
Q

Which vessels are used in CABG?

A

Saphenous VEIN (old)

Internal thoracic (mammary) ARTERY (new)

49
Q

What is PCI?

A

Percutaneous Coronary Intervention

Femoral or radial access to the stenosed vessel for balloon dilation (angioplasty) and stent insertion

Supporting Life (12 decks)

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