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YEAR 2 PHARM WITH ADDITIONS > 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

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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3
Q

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

A

Dihydropyridine receptors

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4
Q

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

A

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

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5
Q

How does the calcium stimulate contraction?

A

It binds to troponin on the thin filament

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6
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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7
Q

What features of contraction is SERCA2a responsible for andwhy?

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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8
Q

What regulates the action of SERCA2a and how does it do this?

A

Phospholamban (PLN)
Phospholamban phosphorylation is stimulated by beta-adrenergic activity
It is a target for phosphorylation by protein kinase A
When dephosphorylated it is an inhibitor of SERCA2a
When phosphorylated it dissociates from SERCA2a and activates the Ca2+ pump
As a result, the rate of cardiac relaxation is increased and, on subsequent beats, contractility is in proportion to the elevation in the size of the SR calcium store

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9
Q

What is phospholamban dephosphorylated by?

A

Protein phosphatase 1

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10
Q

What are the three main channels that are responsible for the action potential in the sinoatrial node?

A 
If channel – hyperpolarisation-activated cyclic nucleotide-gated (HCN) channel 
Calcium channel (T and L type) 
Potassium channel
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11
Q

Describe how these channels are responsible for the action potential of the sinoatrial node.

A

If channel is a sodium channel that opens at the most negative membrane potential
Opening of the sodium channel causes sodium influx, which begins to depolarise the membrane and stimulates the opening of calcium channels, which further depolarises the membrane
Potassium channels are responsible for repolarisation

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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 haveon 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

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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? Name the drugs in each category including their drug class.

A 
Rate slowing  
Phenylalkylamines – verapamil 
Benzothiazepines – diltiazem 
Non-rate slowing  
Dihydropyridines – amlodipine
20
Q

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

A

Reflex tachycardia (baroreceptor reflex)

21
Q

How do organic nitrates cause vasodilation?

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 in angina patients before they exercise

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

23
Q

How do vasodilation and venodilation 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  
Fatigue 
Impotence 
Depression  
CNS effects
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

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
Headaches/flushing
Palpitations

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
Reducing the cAMP in nodal tissue will impact on depolarisation within the AV node

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 by blocking ca channels means that the speed with which the tissue is depolarise is reduced, want to reduce frequency of depolarisations in tachyarrhthymias

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

38
Q

What is the target of cardiac glycosides like digoxin?

A

Na+/K+ ATPase

39
Q

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

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, stimulates para innervation of heart, slowing heart rate -which has a chronotropic effect

40
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

41
Q

What is digoxin used to treat?

A

Atrial fibrillation

Atrial flutter

42
Q

What is an adverse effect of digoxin?

A

Dysrrhythmia

43
Q

What are cardiac inotropes? Name two.

A

They increase the contractility of the heart (it is used in acute heart failure in some cases)
Dobutamine (beta-1 agonist)
Milrinone (phosphodiesterase inhibitor)

44
Q

what is used to treat ventricular arrthymias

A

lidocaine and flecainide

45
Q

what is used to treat complex arrhythimias

A

disopyramide

YEAR 2 PHARM WITH ADDITIONS (33 decks)

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