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LCRS 1 > Drugs and the Cardiovascular System – The Heart > Flashcards

Drugs and the Cardiovascular System – The Heart Flashcards

1
Q

What is the major store of calcium within the cardiomyocyte?

A

Sarcoplasmic reticulum

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2
Q

Channels associated with initiating a heart rate

A

If
ICa Transient
ICa Long lasting
Ik

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3
Q

Chemical associations of If channels

A

Associated with cAMP

Are hyperpolarisation activated cyclic nucleotide gated channels which tend to let in sodium during hyperpolarised times

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4
Q

Role of 2 calcium channels

A

Main drivers behind depolarisation

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5
Q

Role of Ik

A

Initiate repolarisation

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6
Q

The heart has two signalling pathways that are involved in elevating the level of two intracellular second messengers. What are these second messengers?

A

Ca2+ and cAMP

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7
Q

Which plasma membrane proteins allow calcium to enter the cell in response to depolarisation?

A

Dihydropyridine receptors

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8
Q

What happens to the calcium once it has passes into the cell via the dihydropyridine channel?

A

It binds to ryanodine receptors on the sarcoplasmic reticulum and cause calcium release from the SR

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9
Q

How does the calcium stimulate contraction?

A

It binds to troponin on the thin filament

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10
Q

What are the different ways in which calcium is removed from the myoplasm after it has stimulated contraction? Which method is responsible for the majority of calcium removal?

A

Plasma membrane calcium ATPase
Na+/Ca2+ exchanger
SERCA2a (sarcoendoplasmic reticulum calcium ATPase) –responsible for >70% of calcium removal

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11
Q

What features of contraction is SERCA2a responsible for and why?

A

Rate of calcium removal and so it’s responsible for the rate of cardiac muscle relaxation
Size of calcium store, which affects the contractility of the subsequent beat

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12
Q

What are beta adrenoceptors coupled with?

A

Adenylate cyclase – it increases cAMP, which is important in the opening of the If channel to begin depolarisation

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13
Q

How does the parasympathetic nervous system affect heart rate and contractility?

A

It is negatively coupled with adenylate cyclase

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14
Q

What are the determinants of myocardial oxygen supply?

A

Arterial oxygen content

Coronary blood flow

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15
Q

What are the determinents of myocardial oxygen demand?

A

Heart rate
Contractility
Preload
Afterload

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16
Q

What effect do beta-blockers and calcium channel blockers have on the channels responsible for the SA node action potential?

A

Beta-blockers decrease If and calcium channel activity
Calcium channel blockers only decrease calcium channel activity
These 2 affect both HR and contractility

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17
Q

Name a drug that decreases If activity.

A

Ivabradine (blocks the If channel)

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18
Q

What effect does Ivabradine have on contractility?

A

It has no effect on contractility because it doesn’t affect the calcium channels

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19
Q

What are the two types of calcium channel blocker?

A

Rate slowing - cardiac and smooth muscle effects

Non-rate slowing - only really potent in smooth muscle

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20
Q

What is a consequence of non-rate slowing calcium channel blockers?

A

Reflex tachycardia (baroreceptor reflex)

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21
Q

How do organic nitrates cause vasodilation in coronary vasculature?

A

Organic nitrates are substrates for nitric oxide production
The NO then diffuses into the smooth muscle and causes smooth muscle relaxation by activating guanylate cyclase
They are often given in angina patients before they exercise

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22
Q

How do potassium channel openers work?

A

They open the potassium channels and hyperpolarise the vascular smooth muscle so that it is less likely to contract

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23
Q

How do vasodilation and venodilation of nitrates and potassium channel openers reduce myocardial oxygen demand?

A

They reduce the pressure against which the heart is pumping (reduce afterload) and it also causes reduce venous return to the heart (reduced preload) meaning that contractility is decreased

24
Q

As these drugs reduce the myocardial oxygen demand, what condition can they all be used to treat?

A

Angina pectoris

25
Q

State some unwanted effects of beta-blockers.

A 
Bradycardia  
Hypotension  
Hypoglycaemia in diabetics on insulin  
Cold extremities (because of beta-2 blockade) 
Bronchoconstriction
26
Q

Under what circumstance must caution be taken when giving beta-blockers?

A

Cardiac failure – because they reduce heart rate and contractility it can have catastrophic consequences in cardiac failure patients
Reduced CO and increased vascular resistance

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 - due to vasodilation
Headaches/flushing - due to vasodilation in brain
Palpitations- reflex tachycardia

29
Q

What is a simple classification of arrhythmias?

A

Based on its point of origin

Supraventricular, Ventricular and Complex

30
Q

What is the main classification of anti-arrhythmic drugs and how are the drugs ordered?

A 
Vaughan-Williams classification 
I – sodium channel blockers  
II – beta-blockers  
III – prolongation of repolarisation (mainly due to potassium channelblockade) 
IV – calcium channel blockers
31
Q

What is adenosine used to treat?

A

It is used to terminate supraventricular tachycardia

32
Q

How does adenosine work?

A

Adenosine binds to adenosine receptors in the cardiac muscle and vascular smooth muscle
Adenosine receptors are negatively coupled with adenylate cyclase in the heart (A1 receptor) and positively in the vasculature (a2)
Results in relaxation in VSMC and reduced HR and contractility in the nodes

33
Q

What is verapamil used to treat?

A

Supraventricular tachycardia

Atrial fibrillation

34
Q

What is the target of verapamil and how does it work?

A

L-type calcium channel

Reducing calcium entry means that the speed with which the tissue is depolarise is reduced

35
Q

What is amiodarone used to treat?

A

Supraventricular tachyarrhythmia

Ventricular tachyarrhythmia

36
Q

How does amiodarone work?

A

It works by blocking many ion channels
Its main effect seems to be through potassium channel blockade
This prolongs repolarisation, so you’re prolonging the time during which the tissue can’t depolarise

37
Q

Describe re-entry.

A

Some damaged cardiac tissue will make it difficult for depolarisation to pass through it in one direction, but it will allow the action potential to propagate in the opposite direction
This could mean that you get a miniature circuit set up within the tissueand you get re-entry of action potentials so an early contraction

38
Q

How does amioadarone prevent reentry

A

By prolonging the length of repolarisation you decrease the likelihood of tissue in affected area being able to depolarise

39
Q

Adverse affects of amiodarine

A

Remains in body for long time
Thyroid disease
Photosensitive rashes

40
Q

What is the target of cardiac glycosides like digoxin?

A

Na+/K+ ATPase

41
Q

How does digoxin work and what are its effects on the heart and the PSNS?

A

By blocking Na+/K+ ATPase it causes an accumulation of Na+ in the cell
The excess Na+ is then removed by Na+/Ca2+ exchanger, thus increasing the intracellular calcium concentration
This has an inotropic effect
It also causes vagal stimulation which increases refractory period, which has a chronotropic effect

42
Q

What is an important factor to consider before starting treatment with digoxin?

A

Hypokalaemia
Digoxin binds to the potassium binding site on the extracellular component of Na+/K+ ATPase so it competes with potassium for the binding site
If hypokalaemic, there is less competition for digoxin and so the effects of digoxin are exaggerated

43
Q

What is digoxin used to treat?

A

Atrial fibrillation

Atrial flutter

44
Q

Driver behind initial depolarisation in phase 4

A

Pacemaker potential

45
Q

What does SNS affect in heart rate

A

Increase cAMP
If
ICa

46
Q

What does PNS do to affect heart rate

A

Decrease cAMP and increase K

47
Q

Percentage of Ca responsible for binding to troponin

A

EC 25%

SR 75%

48
Q

How is Na conc gradient maintained in myocyte

A

Plasma Na/K pump

49
Q

Drugs influencing heart rate

A

Beta blockers- decrease If and ICa
Calcium antagonists- decrease ICa
Ivabradine- decrease If

50
Q

2 types of rate slowing Ca channels

A

Phenylalkylamines

Benzothiazepines

51
Q

Example of non rate slowing Ca channel antagonist

A

Dihydropyridines- amplodine

52
Q

Example of phenylalkylamines

A

Verapamil

53
Q

Example of benzothiazepine

A

Diltiazem

54
Q

What is an adverse effect of digoxin?

A

Dysrrhythmia

55
Q

Overall effects of digoxin

A

Decreases heart rate to aid with any arrhythmia and increase contractility to improve CO

56
Q

Selectivity of pindolol

A

Equal affinity for b1 and b2 receptors

ISA

57
Q

Selectivity of carvedilol

A

Affinity for both beta adrenoceptors and a1

LCRS 1 (58 decks)

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