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Pharmocology > Drugs of the Cardiovascular system: the Heart > Flashcards

Drugs of the Cardiovascular system: the Heart Flashcards

1
Q

What channels are important in regulation of sinoatrial potential?

A

If - hyperpolarization-activated cyclic nucleotide-gated (HCN) channels

Ica - Transient T-type Ca++ channel or Long lasting L-type Ca ++ channel

Ik - Potassium K+ channels

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2
Q

What are the cells within the SA node?

A
  • primary pacemaker site within the heart

- no true resting potential

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3
Q

What is different about SA node cells compare to other non-pacemaker action potentials in the heart?

A
  • there are no fast Na+ channels and currrents operating in the SA node
  • only HCN channels
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4
Q

What is the job of the If channel?

A
  • it is a sodium channel
  • allows the action potential to propagate
  • opens at the most negative potential and causes a certain amount of depolarisation before calcium channels open
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5
Q

What two forms do calcium channels come in?

A
  • transient

- long-lasting

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6
Q

What is the role of potassium channels?

A

-initiate repolarisation

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7
Q

What mechanism is important in opening if channels?

A

-beta adrenoceptors are linked to adenyl cyclase and lead to an increase in cAMP

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8
Q

What does sympathetic activity do?

A

-increases cAMP and therefore Increased activation of If and Ica channels - increase of Ca

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9
Q

What does parasympathetic activity do?

A
  • negatively coupled with adenyl cyclase
  • promotes the opening of potassium channels
  • prolonged repolarisation
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10
Q

What is stage 4 of the SA node potential responsible for?

A

-spontaneous depolarization that triggers the action potential

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11
Q

What is the mechanism of contracting heart muscle?

A
  • action potential enters from adjacent cells
  • voltage-gated Ca++ channels open, Ca++ enters cells
  • Ca++ induces Ca++ release through ryanodine receptor channels
  • -local release causes a ca++ spark
  • summed ca++ sparks creates a Ca++ signal
  • Ca++ ions bind to troponin to initiate contraction
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12
Q

What is the mechanism for relaxation of heart muscle?

A
  • relaxation occurs when Ca++ unbinds from troponin
  • Ca++ is pumped back into the SR for storage
  • Ca++ is exchanged with Na+
  • Na+ gradient maintained with Na-K+-ATPase pump
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13
Q

What factors determine the myocardial oxygen supply to the heart?

A
  • coronary blood flow

- arterial O2 content

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14
Q

What 4 factors determine the myocardial oxygen demand from the heart?

A
  • HR
  • contractility
  • afterload
  • preload
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15
Q

What is the primary determinant of myocardial oxygen demand?

A

-myocyte contraction

  • increased HR leads to increased contractility
  • increased afterload or contractility = greater force of contraction
  • increased preload = small increase in force of contraction

ALL THESE CONTRIBUTE TO INCREASED WORK

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16
Q

Which drugs decrease HR?

A
  • beta blockers ( decreases If and Ica)
  • calcium antagonists (decrease Ica)
  • Ivabradine (decrease If)
17
Q

Which drugs decrease contractility?

A
  • beta blockers (decrease contractility)

- calcium antagonists (decrease Ica)

18
Q

What are the two classes of calcium antagonists?

A
  • rate slowing (cardiac and smooth muscle actions)

- non-rate slowing (smooth muscle actions - more potent)

19
Q

What are the examples of calcium antagonists?

A

-rate slowing

Phenylalkylamines e.g. Verapamil
Benzothiazepines e.g. Diltiazem

-Non-rate slowing

Dihydropyridines e.g. amlodipine

20
Q

What can non-rate slowing drugs lead to?

A
  • no direct effect on the heart
  • profound dilation can lead to reflex tachycardia
  • reduced peripheral pressure triggers baroreceptors to speed up HR
21
Q

What types of drugs influence myocardial oxygen supply/demand?

A
  • organic nitrates

- potassium channel openers

22
Q

What effects do the organic nitrates and potassium channels openers have?

A
  • increase coronary blood flow
  • vasodilation =decreased afterload
  • venodilation =decreased preload

LESS WORK

23
Q

How does NO work on vascular smooth muscle?

A

-diffuses into vascular smooth muscle and causes relaxation by activating guanylate cyclase

24
Q

What is the treatment plan for angina?

A
  • offer either a beta blocker or calcium channel blocker as first line treatment
  • switch to the other option if the person cannot tolerate the first
  • if the person’s symptoms are not controlled by one try a combination of the two
  • if this is still not working try monotherapy with one of the following : long acting nitrate, ivabradine, nicorandil
25
Q

What are the side effects of beta blockers?

A
  • worsening heart failure ( CO reduction and increased vascular resistance)
  • Bradycardia ( heart block and decreased conduction through AV node)
  • cold extremities (loss of B2 receptor mediated cutaneous vasodilation in extremities)
  • fatigue
  • impotence
  • depression
  • CNS effects e.g. nightmares
26
Q

What other conditions do you have to be careful about before giving beta blockers?

A
  • asthmatic- inhibits B2 action of bronchodilation

- diabetes - they interfere with actions of the liver masking hypoglycaemia

27
Q

What are the side effects of verapamil?

A
  • bradycardia and AV block

- constipation

28
Q

What are the side effects of dihydropyridines?

A
  • ankle oedema
  • headache/ flushing
  • palpitations

due to vasodilation/reflex adrenergic activation

29
Q

What are the aims of rhythm disturbance treatment?

A
  • reduce sudden death
  • prevent stroke
  • alleviate symptoms
30
Q

How are arrhythmias classed?

A

based on location

  • supraventricular
  • ventricular
  • complex (combination of the two)
31
Q

What is the Vaughan-Williams classification of anti-arrhythmic drugs?

A 
class I - sodium channel blockade
class II - beta adrenergic blockade 
class III - prolongation of repolarisation (membrane stabilisation mainly due to potassium channel blockade)
class IV - calcium channel blockade
32
Q

What are the limitations of Vaughan -Williams classification?

A
  • rare that a drug only fits into one category

- clinical significance is limites

33
Q

What are the uses and mechanism of action of adenosine?

A
  • IV to terminate supraventricular tachyarrhythmias
  • short lived
  • safer than verapamil

binds to A1 receptors, cAMP reduces and so reduced contraction

34
Q

What are the uses and mechanism of action of verapamil?

A
  • reduction of ventricular responsiveness to atrial arrhythmias
  • depresses SA automaticity and subsequent AV node conduction
35
Q

What are the uses, mechanism of action and side effects of amiodarone?

A
  • superventricular and ventricular tachyarrhythmias, often due to re-entry
  • complex action involving multiple ion channel block

it accumulates in the body and leads to photosensitive skin rashes, hypo/hyperthyroidism, pulmonary fibrosis

36
Q

What are the uses and mechanism of action of digoxin?

A

-atrial fibrillation and flutter

  • inhibition of the Na-K-ATPase pump, results in increased intracellular Ca++ and causes a positive inotrophic effects
  • central vagal stimulation causes increased refractory period and reduced rate of conduction through the AV node
  • side effects - dysrhythmias
37
Q

why does hypokalaemia lower the threshold for digoxin toxicity?

A

-digoxin binding site is the same as the potassium binding site, if potassium falls digoxin is more likely and available to bind to that target

Pharmocology (16 decks)

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