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MD3001 NG > treatment of angina > Flashcards

treatment of angina Flashcards

1
Q

what 3 things effect the window for coronary flow?

A
  • increased hr
  • increased ventricular pressure (due to volume increase/ can’t fill swell)
  • decreased aortic pressure
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2
Q

cause of angina

A

Chemically, angina is thought to be caused by the build-up of chemical factors (e.g adenosine) due to increased metabolism of the tissue and lack of blood supply to give nutrients and take away waste products produced by this increased metabolism

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3
Q

what are the 3 causes that shrink the coronary window and their examples?

A

1- shortening diastole (increased hr)
2- increased ventricular end and diastolic pressure (aortic valve stenosis- this will cause incomplete emptying which increases ventricular pressure- you don’t get the same volume of blood pushed out.)
3- reduced diastolic arteriole pressure (mitral or aortic valve incompetence, heart failure- regurgitation of blood, not enough force)

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4
Q

what is demand ischaemic?

A

specific type of ischamia where the oxygen requirement of the myocardium are not being met due to some increased need

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5
Q

what is coronary ischaemia usually a result of and what may it cause?

A
  • result of atherosclerosis
  • cause angina
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6
Q

cause of sudden iscahemia and as a result of what?

A
  • caused by thrombosis
  • result in cardiac infarction
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7
Q

during ischaemia, what happens to calcium levels?

A

(cellular calcium overload) release of a high conc of calcium which will change the excitability in the local region = dysrhythmias or cell death

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8
Q

what do coronary spasms sometimes cause?

A

angina

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9
Q

what is angina pectoris?

A
  • chest pain due to inadequate supply of oxygen to the heart
  • typically severe and crushing
  • tight constricting, dull or heavy
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10
Q

what are the characteristic distribution of pain in angina pectoris?
what is it Brought on by?
what is responsible for the pain?

A
  • retrosternal, or left side of chest and can radiate down the left arm, neck, jaw and back
  • Brough on by exertion, cold or excitement
  • chemical factors that cause pain in skeletal muscle are though to be the cause (K, H and adenosine)
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11
Q

what can angina accompany or be a precursor of?

A

heart attack

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12
Q

angina?

A

temporary disturbance in blood flow to the heart that will not cause permenant damage.
unstable anima (if not treated) can lead to a heart attack.
both are caused by coronary heart disease

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13
Q

3 classes of angina?

A
  • printzmetals variant angina
  • chronic stable angina
  • unstable angina
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14
Q

printzmetal’s angina?

A
  • caused by vasospasm
  • supply ischaemia
  • uncommon
  • caused by coronary artery spams (vasospasm) - random spasms of the vasculature I the heart which can block blood supply
  • not completely understood but associated with atherosclerosis
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15
Q

chronic stable angina?

A
  • caused by fixed narrowing of the coronary vessels
  • fixed stenosis
  • demand ischaemia
  • predictable chest pain on exertion
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16
Q

unstable angina?

A
  • supply ischaemia
  • occurs at rest with less exertion than stable angina
  • associate with a thrombus around a rupturing atherosclerotic plaque but without complete occlusion of the vessel.
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17
Q

treatment to reduce chest pain symptoms?

A
  • beta blockers
  • nitrates
  • calcium channel antagonists
  • nicroandril
  • ivabradine
  • ranolazine
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18
Q

treatment for prolonged survival of angina?

A
  • beta blockers
  • aspirin (blood thinning)
  • statins (lipid lowering, reduced atherosclerotic complications)
  • angiotensin converting enzyme inhibitor
  • angiotensin II receptor blocker
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19
Q

different types of treatment for the symptoms?

A

1- offer short acting nitrates for preventing and treating episodes of angina

2- offer first line treatment = beta blocker or calcium channel blocker

3- if control by B-blockers isn’t that good, add CCB

4- if both are not working optimally, use other drugs like nicorandril or ivabradine.

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20
Q

how do antianginal drugs work?

A
  • ## mainly work by decreasing the metabolic demand of the muscle
21
Q

what are the antianginal drugs that are vasodilators?

A
  • organic nitrates
  • nicorandril
  • calcium antagonists

they will decrease the preload or after load (decrease the force that heart has to exert to move blood out)

22
Q

how does beta blockers and ivabradine work as antianginal drugs?

A
  • they will slow down the hr
  • they decrease the metabolic demand of the muscle
23
Q

what are the 2 types of organic nitrates?

A

glyceryl trinitrate (shorter acting)
isosorbide mononitrate

24
Q

how do the 2 organic nitrates work?

A
  • decrease preload by dilation of the venous system
  • vasodilators
  • work by being metabolised to NO and relax smooth muscle (in particular vascular smooth muscle)
  • act on veins to decrease cardiac preload
  • decrease in cardiac workload is helped by dilation of collateral coronary vessels
25
Q

what will have to happen for organic nitrates to work on arteries swell?

A

higher concentration can effect arteries and therefore decreasing the after load

26
Q

the decrease in cardiac workload from organic nitrates will cause what?

A
  • it will improve the distrubution of coronary blood flow towards ischaemic areas
  • dilation of constricted vessels is particularly beneficial in variant angina.
27
Q

describe the clinical use of organic nitrates for stable angina?

A

prevention by sublingual glyceryl trinatrate shortly before exertion or isosorbide mononitrate long before

28
Q

describe the clinical use of organic nitrates in unstable angina?

A

intravenous glyceryl trinitrate

29
Q

what are the side effect of organic nitrates

A
  • headache (decreased venous return and cardiac output)
  • postural hypotension
30
Q

what are the 2 other clinical uses of organic nitrates?

A
  • acute heart failure = give intravenous gyleryl trinatrate
  • chronic heart failure = give isosorbide mononitrate with hydralazine in patients of African American background.
31
Q

what is different about African American patients and why they get slightly different treatment?

A

because they are subject to epithelial sodium channel differences

32
Q

beta blockers?

A
  • important in the first line treatment
  • important in the prophylaxis and treatment of stable and unstable angina
  • bisoprolol, atenolol
33
Q

hw to BB work?

A

decrease cardiac oxygen consumption by slowing the heart rate
- they also have an antidysryhtmic action which reduced cell death/death after MI

34
Q

how do calcium channel blockers work?

A
  • they prevent the opening of voltage gated L-type calcium channels
  • blocking the entry of calcium
  • this mainly effects the heart and smooth muscle to inhibit calcium entry upon muscle cell depolarisation
35
Q

what are the 2 main types of calcium channel blockers?

A
  • dihydropyridine derivatives (eg amlodipine and lercanidipine)
  • rate limiting (eg verapamil and diltiazem)
36
Q

describe the vasodilator effect of calcium channel blockers?

A
  • it is mainly on resistance vessels
  • reduces the after load
  • also dilates coronary vessels (important in variant angina)
37
Q

what can verapamil and diltiazem be used for?

A

it can reduce and impair AV conduction and myocardial contractility

38
Q

what are the clinical uses of CCB in angina:
when would you use amlodipine or lercandipine?

A

the choice between any of the 4 drugs will depend on combirbidity and drug interactions:

  • it is safe in patients with heart failure, it will be used instead of beta blockers in prinzmetal angina or alongside beta blockers in most angina.
39
Q

what are the clinical uses of CCB in angina:
when would you use diltiazem or verapamil?

A

the choice between any of the 4 drugs will depend on combirbidity and drug interactions:

  • they can be used but are contraindicated in her failure, bradycardia, AV block or in the presence of Beta blockers.
40
Q

side effects of CCB

A

headache
constipation
ankle oedema (decreasing resistance, increasing flow down to ankle, change in frank starling forces)

41
Q

2 other clinical uses of CCB?

A

1- antidysrhymias (mainly verapamil)
- slows ventricular rate in rapid atrial fibrillation
- prevents recurrence of supra ventricular tachycardia (SVT)
- no effect on ventricular arrhythmias

2- hypertension (elevated after load)
- mainly amlodipine or lercanidpine

42
Q

what drug is a potassium channel activator and how does it work?

A

nicroandril
- combines activation of potassium ATP channel with nitrovasodilator actions
- causes hyperpolarisation of vascular smooth muscle (decreases the likelihood of vascular contraction, moves towards resting membrane potential)
- both an arterial and venous dilator

43
Q

nicorandril side effects?

A

headaches
flushing
dizziness

44
Q

when would nicorandril be used?

A

in patients who remain symptomatic despite optimal management with other drugs

45
Q

2 other anti-anginals?

A

1- ivabradine
2- ranolazine

46
Q

ivabradine

A

= inhibits funny ‘f’type channel in heart
reduces cardiac pace maker activity
therefore inhibits heart rate

47
Q

ranolazine?

A

unique anti-anginal used as a last resort
influences Na
- decreases calcium in cells
- decreases contractility
- decrease hr

48
Q

preload?

A

the force that stretches the cardiac muscle prior to contraction., with greater volumes of blood providing greater stretch

49
Q

afterload?

A

the pressure of systemic vascular resistance in the aorta that the left ventricle has to pump against in order to push blood into systemic circulation

MD3001 NG (56 decks)

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