L8 - Angina Flashcards

1
Q

What is ischaemia? What can it lead to?

A
  • interruption of cardiac blood supply due to blocked in vessels, primarily involving coronary vessels
  • lack of nutrients and oxygen leading to tissue death
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2
Q

Why does ischaemia occur?

A
  • as a consequence of atherosclerosis (coronary artery disease)
  • plaque build-up in vessels causing blockage
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3
Q

What is the spectrum of ischaemic heart disease?

A

early stages: angina

later stages: acute MI

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4
Q

What is angina?

A

pain in chest caused by decreased blood supply to myocardium due to atherosclerosis
- it can be a symptom of coronary artery disease

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5
Q

What is atherosclerosis?

A

hardening and narrowing of arteries due to plaque formation (deposition of fatty material in arteries)

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6
Q

What are the 4 stages of cardiovascular disease?

A
  • normal
  • fatty streak
  • fibrous plaque
  • advanced plaque
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7
Q

describe the 1st stage of CVD

A

NORMAL

  • normal blood flow and BP
  • exposed to risk factors
  • initial lesion occurs = macrophage infiltration
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8
Q

What are the risk factors of CVD?

A
  • diet
  • inflammation
  • poor oral health
  • hypertension
  • diabetes
  • smoking
  • weight
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9
Q

describe the 2nd stage of CVD

A

FATTY STREAK

  • accumulation of lipid-filled white blood cells including active WBC and “dead” cells containing cholesterol
  • reduce elasticity of artery walls but doesn’t affect blood flow for decades
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10
Q

describe the 3rd stage of CVD

A

FIBROUS PLAQUE

  • hardening of the arteries (calcification of fatty streak)
  • plaque continues to progress and expand
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11
Q

describe the 4th stage of CVD

A

ADVANCED PLAQUE

  • lumen so narrow blood can’t flow through anymore
  • plaque becomes unstable and breaks off
  • initiates clotting cascade
  • can turn angina into MI
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12
Q

What are the types of angina?

A

Stable angina
- chest pain occurs when heart is working hard and needs more oxygen (stress and exercise)
- caused by narrow arteries
Unstable angina
- new chest pain or change in usual pattern of chest pain
- cause by clot formation

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13
Q

What are the 3 things involved in the management of stable angina?

A
  • dilation of coronary arteries (increase blood supply)
  • control HR and force of contraction (reduce work load of heart)
  • reduce CV risk factors
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14
Q

What is the 1st line treatment for acute attacks?

A

GTN - dilation of coronary arteries

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15
Q

What drug class is GTN and how does it work?

A
  • nitrate
  • mimics endogenous NO and causes non-specific vasodilation
  • increases blood supply to the heart (coronary arteries) and reduces cardiac work (venous dilation)
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16
Q

How is GTN administered?

A
  • sublingual spray

- rapid onset + short lived

17
Q

How does NO cause vasodilation?

A
  • acts on vascular smooth muscle to increase guanylate cyclase activity
  • increased cGMP activates kinases
  • promotes smooth muscle relaxation
  • cGMP terminated by phosphodiesterase (PDE5)
18
Q

What are the side effects of GTN?

A

dose related side effects:

  • hypotension
  • headaches
  • flushing
  • reflex tachycardia
19
Q

When is GTN used?

A

first line treatment for acute angina attacks

20
Q

What are other treatments for angina? (chronic treatment)

A

beta blockers or calcium channels blockers- control HR and force of contraction

21
Q

What are beta blockers? What is a feature of them?

A

B adrenergic receptor antagonists
- their degree of response is proportional to the level of sympathetic stimulation i.e. increased response in disease state, exercise, stress

22
Q

selective/non-selective B blockers: where do they act?

A

non-selective: block B1 and B2 receptors

selective: B1 receptors

23
Q

What are three B blockers and how are they different?

A

propranolol: non-selective B blocker, cross BBB
metoprolol: B1 selective, cross BBB
atenolol: B1 selective, cannot cross BBB

24
Q

What are B blockers used for?

A
  • primarily angina
  • tachycardia
  • hypertension
    not 1st line in combination with diuretic
25
Q

What are the adverse effects of B blockers?

A
B1 mediated:
- fatigue/ poor exercise tolerance
- CNS effects (if cross BBB)
B2 mediated:
- bronchoconstriction in lungs
- worsening lipid profiles
- hypoglycaemia
- increased toxicity in elderly
26
Q

How do CCBs work?

A

they inhibit Ca2+ influx through L-type calcium channels

27
Q

What effect do CCBs have on different parts of the heart?

A
  • cardiac muscle: reduce force of contraction
  • SA nodal tissue: reduce rate of contraction
  • AV node: decrease conduction velocity
28
Q

What are the 2 types of CCBs? What makes them different?

A
  • cardiac specific: require open channel in order to bind and block the pore = able to act in the heart because channels frequently open
  • vessel specific: stabilises inactive channel = only able to act in vessels where channels less frequently open
29
Q

What are the cardiac and vessel selective CCBs?

A

verapamil and diltiazem

30
Q

What is the vessel specific CCB?

A

nifedipine

31
Q

What are the cardiac specific CCBs used for and why?

A
  • mainly angina
    because increase oxygen supply and decrease oxygen demand
  • hypertension
    causes vasodilation and reduces HR and force of contraction
  • tachycardia
    reduces HR and slows contraction of the heart
32
Q

What are the adverse effects of cardiac specific CCBs?

A
  • generally well tolerated
  • most side effects vascular related e.g. flushing
  • dose-related effects e.g. hypotension + bradycardia
    can cause cardiac depression if used with B blockers
33
Q

What is the vessel specific CCB used for?

A
  • newer 1st line treatment for hypertension especially in elderly with vessel stiffness
34
Q

What are the side effects of vessel specific CCBs?

A
  • don’t use alone in angina because causes reflex tachycardia and increased workload on heart
  • most are dose dependent e.g. hypotension, flushing, dizziness + headache