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CVS > Pharmacology of the CVS > Flashcards

Pharmacology of the CVS Flashcards

1
Q

What is angina pectoris caused by?

A

Local myocardial ischaemia
o Oxygen demand exceeds supply
o Often precipitated by exertion, reversible on rest

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2
Q

What are the symptoms of angina pectoris?

A

o Crushing chest pain
 Also, in jaw, shoulder, arms
o Ischaemic products (e.g. Lactate, H + ) stimulate sympathetic nociceptive
afferents
o May also be associated with shortness of breath, sweating, nausea

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3
Q

What increases risk of an angina attack

A

Increased systolic blood pressure (afterload)
Increases heart rate
Increases contractility
Increased vasoconstriction

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4
Q

How is stable angina induced?

A

Exercise-induced – predictable

Not able to meet increased O 2+ demands due to atheroma in coronary arteries

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5
Q

How is stable angina relieved?

A

Relieved by rest and medication

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6
Q

What is unstable angina indduced by?

A

Exercise-induced with minimal exertion – unpredictable

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7
Q

What may unstable angina indicate?

A

May indicate thrombosis, plaque rupture

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8
Q

When do the symptoms express themselves in variant angina?

A

Symptoms at rest

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9
Q

Due to what reason is there a reduced supply of O2 in variant angina?

A

Decreased O 2 supply due to vasospasm (un-controlled vasoconstriction, decreasing
blood flow) downstream of occlusion

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10
Q

What are the aims of treatment of angina?

A 
Improve Prognosis
- Prevent MI & death
- Reduce plaque progression
- Stabilise plaque
- Prevent thrombosis
Minimise symptoms
- Improve quality of life
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11
Q

Treatment of angina(Beta-blockers) What are the effects?

A
  • Decreases rate
  • Decreases contractility
  • Decreased oxygen deman
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12
Q

Treatment of angina(Calcium channel blockers) What are the effects?

A

Dilate arteriolar vessels

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13
Q

Treatment of angina(Nitrates) What are the effects?

A

Dilate arteriolar vessels

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14
Q

What action do beta blockers reduce?

A

Reduce actions of sympathetic activity (noradrenaline & adrenaline) on β1
adrenoreceptors in the heart

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15
Q

What do beta blockers slow down?

A

Slow heart rate and AV conduction

o Increase diastolic time – increase coronary artery perfusion

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16
Q

What force does beta blockers reduce?

A

Reduce force of contractility

o Reduce myocardial work and oxygen consumption

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17
Q

What is atenolol more selective of?

A

Atenolol (more β1 selective – β2 found in vasculature and airways)

18
Q

Side effects of beta blockers

A

bronchospasm, fatigue, postural hypotension

19
Q

When are beta blockers contraindicated?

A
  • Asthma – block β2 receptor can cause constriction & bronchospasm
  • Heart block where atrial-ventricular conduction is poor – may block AV node
20
Q

What do calcium ion channel blockers do?

A

Drugs which can block VGCC’s and prevent Ca 2+ entry thus reducing the force of
contraction in ventricular myocytes

21
Q

What do calcium ion channel blockers cause?

A

This causes vasodilation in vascular smooth muscle

22
Q

What changes do calcium ion channel blockers bring about?

A

Reduce Ca 2+ entry into cardiac myocytes / vascular smooth muscle cells – reducing
contractility
o Direct coronary vasodilation – more coronary blood flow
o Reduce TPR / BP / afterload – heart works less hard to eject blood
o Reduce force of contraction – less O 2 consumption

23
Q

What are the 3 subtypes of Ca2+ channel blockers?

A

Dihydropyridines (vascular) – Amlodipine, Nifedipine

Benzothiazepines (cardiac) – Verapamil

Diphenylalkyamines (both) – Diltiazem

24
Q

What can blocking Ca2+ channels alter?

A

blocking Ca 2+ channels in the heart may alter electrical conduction and contractility

25
Q

What does NO form?

A

Forms PKG

26
Q

How does PKG formed from NO reduce smooth muscle tone?

A
  • Myosin light chain dephosphorylation
  • Increase uptake of Ca2+ by SR causing a decrease in cytoplasmic levels
  • Active K+ channels causing hyperpolarisation and closing VGCC
27
Q

What does coronary artery dilation increase?

A

Increases collateral arteriole dilation to shunt blood from areas of good perfusion
to poor perfusion (between functional end-arteries)

28
Q

What does venodilation decrease?

A

Decrease in venous return / pre-load

29
Q

What does arteriole dilation decrease?

A

Decrease in TPR / afterload

30
Q

What 2 factors reduce myocardial O2 demand?

A

A decrease in preload and afterload reduces myocardial O 2 demand

31
Q

What happens when NO combines with viagra?

A

You also have to be careful when combined with Sildenafil (Viagra) because a PDE5 inhibitor
and nitrates can produce significant hypotension

32
Q

What are other commonly prescribed anti-angina drugs?

A

Aspirin
Clopidogrel
Nicorandil
Statins

33
Q

What does aspirin inhibit and decrease?

A

Inhibits COX

- Decreases thromboxane A 2 and platelet aggression

34
Q

What does clopidogrel inhibit?

A

Inhibits ADP receptor on platelets, reduces aggregation

35
Q

What do both aspirin and clopidogrel reduce?

A

Both of these drugs reduce thrombosis and can be used together as they have entirely
different mechanisms

36
Q

What do nicorandil activate and causes what??

A

Potassium channel activator

Causes Hyperpolarisation

37
Q

When is nicorandil used?

A

It is used if β-blockers, Ca 2+ channel blockers are insufficient

38
Q

What do statins inhibit and lower?

A

HMG Co-A reductase inhibitor

Lowers cholesterol levels

39
Q

What is Ivabradine a selective inhibitor of?

A

Selective inhibitor of I f (funny current) channel in the sino-atrial node

40
Q

What does Ivabradine decrease?

A

Decreases pacemaker potential frequency

- Decreases heart rate to reduce myocardial O 2 demand

CVS (17 decks)

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