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ZA - Cardio Diseases > Stable Angina and Anti-Angina Drug Pharmacology > Flashcards

Stable Angina and Anti-Angina Drug Pharmacology Flashcards

1
Q

What is angina and what is it caused by?

A

Chest pain due to reduced coronary artery blood flow

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2
Q

Describe the feeling and location of angina pain.

A

Tight-band/crushing pain
Retrosternal
Radiates to jaw or left arm

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3
Q

Lying down eases angina pain - true or false?

A

False - makes it worse, eases upon sitting forward

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4
Q

When does angina normally happen?

A

When myocardial O2 demand increases - exertion, cold weather, large meal etc

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5
Q

What three things regarding coronary arteries can cause angina? - place in order of how common.

A

Coronary atheroma

Coronary artery spasms

Coronary inflammation

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6
Q

What else causes angina which is uncommon?

A

Reduced O2 transport - anemia

Increased O2 demand - LVH or thyrotoxicosis

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7
Q

What are the non-modifiable risk factors for angina?

A

Gender - Males and post-menopausal females

Age
Genetics/Family history

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8
Q

What are the modifiable risk factors?

A

Hypertension
Hyperlipidaemia
Hyperglycaemia
Smoking

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9
Q

What symptoms do you look for in a history of a patient with suspected angina?

A

Dyspnoea and fatigue on exertion
Syncope on exertion
Chest pain -restrosternal radiating to left arm/jaw

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10
Q

What signs might be present?

A 
Tar stains - smoker
Obesity 
xanthalasma and corneal arcus 
Hypertension
Bruits
Abdmonial aortic aneurysm
Absent or reduced peripheral pulses 
Retinopathy
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11
Q

What’s retinopathy?

A

Damage to retina

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12
Q

Name the investigations?

A 
Blood checks
CxR
ECG
ETT
Myocardial perfusion imaging
Invasive angiography
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13
Q

What to look for in bloods?

A

FBC
Lipid profile
Fasting glucose
Us and Es

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14
Q

What to look for in a CxR?

A

Can exclude other causes of chest pain such as pulmonary oedema

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15
Q

What to look for in ECG?

A

Pathological Q-waves

LVH - ST depression

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16
Q

What makes an ETT positive?

A

Angina symptoms with St-segment depression on exertion relatively quickly

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17
Q

Does a negative ETT mean that angina is excluded?

A

No - but if there was a high workload prognosis is good

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18
Q

Myocardial perfusion imagine - better or worse at detecting CAD?

A

Better as it shows localisation of ischemia and size of area affected

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19
Q

What are some negatives of myocardial perfusion imaging?

A

Expensive

Uses radiation

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20
Q

How is myocardial perfusion imaging carried out?

A

Stress applied to patient via exercise or pharamlogically

Tracer injected via IV twice - at rest and at peak stress

Two reading compared

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21
Q

When does myocardial perfusion imaging show ishchaemia?

A

If tracer seen at rest but not at peak stress

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22
Q

When does myocardial perfusion imaging show infarction?

A

If tracer is not seen at all in both readings

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23
Q

When would invasive angiography be used?

A

If there is a strongly positive ETT suggesting multivessel disease

If angina won’t clear with meds

If diagnosis still not clear

If patients are young

If there is a high occupational risk with patients - like a driver having an angina attack and crashing

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24
Q

How is invasive angiography carried out?

A

Cannula inserted into radial or femoral arteries, passed to aortic root and into ostium of coronary arteries

Contrast is injected and an image of vessel lumen is viewed on an x-ray

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25
Q

Severity: Stage 1?

A

Symptoms only on significant exertion - none on rest

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26
Q

Severity: Stage 2?

A

Slight limitation of daily activities - symptoms on walking more than 1 flight of stairs

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27
Q

Severity: Stage 3?

A

Marked limitation of daily activities - symptoms on only one flight of stairs

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28
Q

Severity: Stage 4?

A

Symptoms on the most basic activities such as washing or getting dressed

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29
Q

What are the steps in a medical treatment regime?

A

1 - Prescribe a short acting nitrate - GTN spray
2 - Beta blockers or CCBs
3 - Swap between beta blockers and CCBs or use both together
4 - revascularisation

30
Q

How do nitrates work?

A

Vasodilators - relax smooth muscle by releasing cAMP
Venodilatiors - reduces venous return

This reduces preload and afterload which reduces myocardial O2 demand

31
Q

Do nitrates relieve coronary vasospasm?

A

Yes

32
Q

Adverse drug reactions of nitrates ?

A

Headache

Hypotension - GTN syncopes

33
Q

What is step 2 in a treatment regime?

A

Prescribe either B.blockers or CCBs

34
Q

Name some beta blockers?

A

Bisoprolol

Atenolol

35
Q

How do beta blockers work?

A

They are rate limiting drugs
Block B1 and B2 receptors which blocks noradrenaline or adrenaline binding to it.
There for it blocks the sympathetic response

36
Q

What do beta blockers reduce?

A 
HR
Force of contraction
Velocity of contraction
CO
BP
37
Q

What do beta blockers protect myocytes from?

A

O2 free radicals during ischaemic period

38
Q

Beta blockers increase exercise threshold - T or F

A

True

39
Q

Contraindictions of beta blockers?

A

Asthma - (Blocks B2 agonist response)

Peripheral vascular disease

Heart failure - these patients depend on sympathetic drive

Bradycardic patients - causes heart block

40
Q

Adverse drug reactions of beta blockers?

A

Tiredness
Bradycardia
Rebound - if taken off suddenly can induce a MI

41
Q

Drug - Drug interactions of beta blockers?

A

Anti-hypertensive agents - hypotension
Rate limiting drugs - bradycardia/heart failure
NSAIDS - blocks anti-hypertensive actions
Insulin - masks effects

42
Q

How do CCBs work?

A

Block L-type channels

43
Q

What are the 2 types of CCBs - name some drugs for each

A

Rate limiting - verapamil and diltiazem

Vasodilating - amlodipine felodipine

44
Q

What is the purpose of using CCBs?

A

Both types work to reduce myocardial O2 demand (rate limiting) and workload (vasodilating)

45
Q

Contraindictions of CCBs?

A

Don’t use nifedipine as its a rapid vasodilator and can cause a stroke/MI
Post MI patients as can increase morality/morbitiy
Unstable angina

46
Q

Adverse drug reactions for CCBs?

A

Ankle oedema which doesn’t respond to diuretics

Headache
Flushing
Palpitations

47
Q

Adverse drug reactions of just rate limiting CCBs?

A

Bradycardia

Constipation

48
Q

What is step 3 in treating angina?

A

Swap between B.Blocker or CCB

or

Use both together

49
Q

What is step 4?

A

Consider revascularisation

50
Q

In patients with atherosclerotic plaques - what other drugs should we give as a routine?

A

Aspirin/Clopidogrel

Statins

51
Q

How does aspirin work?

A

Anti-platelet aggravater

Inhibits platelet thromboxane production which makes platelets

52
Q

Whats a bad side effect of aspirin?

A

Causes bleeds - especially GI - be wary when giving to elderly

53
Q

How does clopidogrel work?

A

Also stops platelet aggregation

Inhibits ADP platelet activation

54
Q

Side effects of clopidogrel?

A

Also causes bleeds - not as much in GI though

55
Q

How do statins work?

A

HMG Co-A reductase inhibitors

Reduce cholesterol

56
Q

If a patient cannot take b.blockers or CCBs - what is some alternative treatment?

A

Long acting nitrates
Ivabradine
Nicorandil
Ranolazine

57
Q

Desribe long acting nitrates

A

Isosorbide mono/di nitrate

Sustained release via tablets

58
Q

Whats a problem with long acting nitrates and how is it overcome?

A

Tolerance quickly develops

Give doses at 8am and 2pm for a sustained release period followed by a nitrate free period

59
Q

How does ivabradine work?

A

Sinus node inhibitor
Rate limiting

Slows the diastolic depolarization of sinus node

60
Q

How does nicorandil work?

A

K+ channel opener
Also known as a preconditioner

The influx of k+ stops the influx of Ca2+ into cells giving a negative inotropic response, vasodilation and venodilation

61
Q

What does inotropic mean?

A

Force of contraction

62
Q

Surgical treatment - how does PCI work?

A

Same as invasive angiography - but a balloon and stent are placed in the vessel to “widen” it and squash the plaque

63
Q

What drugs must be given if a stent is placed in the artery?

A

Aspirin and clopidogrel to stop platelet activation until the body no longer regards the stent as a foreign opject

This stops thrombosis

64
Q

Does stenting cure the disease?

A

No - it only really deals with symptoms

65
Q

Risks of PCI and stenting?

A

Re-stenosis
Emergency CABG
MI
Death

66
Q

When is a CABG used?

A

When there is a mutlivessel disease or the anatomy is unsuitable for PCI

67
Q

Does CABG have a longer lasting benefit?

A

Yes - but graft can begin to deteriorate after 10 years

68
Q

What subgroups benefit more from a CABG?

A

If there is a 70% stenosis of the left main stem artery

If there is a 3 vessel CAD

A 2 vessel CAD with either significant stenosis of left main stem artery or less than 50% ejection fraction

69
Q

Describe the CABG procedure.

A

Long saphenous vein (commonly used) or mammary artery taken

If a vein needs to be reversed so valves face the right way

Attached to aorta distal to site of blockage to BYPASS it

70
Q

IS CABG safer than PCI?

A

Yes - fewer risks BUT these risks are higher

71
Q

What are the risks of CABG?

A

Death

Q-wave MI

ZA - Cardio Diseases (36 decks)

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