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Y2 LCRS Pharm Fwong > 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
Basically different pathways can eventually trigger these 2 secondary messengers. Different messengers have different functions (some functions overlap eg cAMP and Ca2+ both involved in contractility control)

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

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7
Q

What features of each heart beat is the SERCA2a responsible for?

A

The activity of SERCA2a is responsible for the removal of >70% of myoplasmic Ca2+ in humans
As a result, SERCA2a determines both:
1. the rate of Ca2+ removal and consequently the rate of cardiac muscle relaxation
2. and the size of the Ca2+ store (which affects cardiac contractility in the subsequent beat

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8
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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9
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 (transient then long lasting type), which further depolarises the membrane
Potassium channels are responsible for repolarisation

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10
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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11
Q

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

A

m2 receptors in the heart are Gi receptors which decrease cAMP (negatively coupled with adenylate cyclase).

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12
Q

What are the determinants of myocardial oxygen supply?

A

Arterial oxygen content

Coronary blood flow

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13
Q

What are the determinents of myocardial oxygen demand?

A

Heart rate
Contractility
Preload
Afterload

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14
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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15
Q

Name a drug that decreases If activity.

A

Ivabradine (blocks the If channel)

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16
Q

What effect does this drug have on contractility?

A

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

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17
Q

What are the two types of calcium channel blocker? Name the drugs in each category including their drug class.

A

1.Rate slowing/rate limiting/non-dihydropyridines (blocks calcium channels in Cardiac + smooth muscle actions)
Phenylalkylamines (e.g. Verapamil)
Benzothiazepines (e.g. Diltiazem)

Non-rate slowing/ dihydropyridines(only blocks calcium channels in smooth muscle of blood vessels – more potent)
Dihydropyridines (e.g. amlodipine)

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18
Q

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

A

Reflex tachycardia (baroreceptor reflex)

19
Q

How do organic nitrates cause vasodilation?

A

Organic nitrates release NO which leads to smooth muscle relaxation. (they promote cGMP production which causes relaxation). They also promote K+ efflux which leads to hyperpolarisation. Hyperpolarisation decreases Ca2+ influx and hence less contraction.

20
Q

How do potassium channel openers work?

A

Potassium channel openers promote K+ efflux and hence hyperpolarization which reduces Ca2+ influx into the VSMC and hence less contraction. This is because the transient and long lasting type Ca channel are both examples of voltage gated calcium channels.

21
Q

How do vasodilation and venodilation reduce myocardial oxygen demand?

A

They reduce the pressure against which the heart is pumping (reduce afterload)
Venodilation allows more pooling of blood in veins and hence reduced blood volume going back to the heart (reduced preload)

22
Q

As these drugs (K channel opener, non rate limiting and rate limiting CCBs etc) reduce the myocardial oxygen demand, what condition can they all be used to treat?

A

Angina pectoris

23
Q

State some unwanted effects of beta-blockers.

A
  • increased TPR due to blockage of B2 mediated vasodilation
  • CO reduction (if you overdo it)
  • b2 blockage = cold extremities
  • Blocks airway smooth muscle relaxation (B blockers contra indicated in asthmatics)
  • blocks glucose regulation in liver (contraindicated in diabetics)
Other: (validity of these are unclear)
Fatigue
Impotence (sexual dysfunction)
Depression
CNS effects (lipophilic agents) e.g. nightmares
24
Q

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

A

Cardiac failure – because they reduce heart rate and contractility and so B blockers can make it worse it can have catastrophic consequences in cardiac failure patients
Contraindicated in asthmatics and diabetics as well (see last card)

25
Q

What are the side effects of verapamil (a rate limiting CCB)?

A
  • Bradycardia and AV block (too much Ca2+ channel block, this happens when you take it chronically and their effects can build up)
  • Constipation (blocked Gut Ca2+ channels,=reduced motility)
26
Q

What are the side effects of dihydropyridines?

A
  • Ankle oedema - vasodilation allows more blood into capillary beds and so increased hydrostatic pressure
  • Headaches/flushing - vasodilation in brain and peripheral vasodilation causes flush
  • Palpitations- baroreceptor reflex due to reduced TPR
27
Q

What is a simple classification of arrhythmias?

A

Based on its point of origin

Supraventricular, Ventricular and Complex

28
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
29
Q

What is adenosine used to treat?

A

It is used to terminate supraventricular tachycardia

30
Q

How does adenosine work?

A

VSMC:
Bind to A2 (adenosine 2) receptors and stimulates cAMP to cause relaxation. (B2 also uses cAMP to cause relaxation)

SAN and AVN:
Bind to A1, decreases cAMP and slows the heart down. Nb this is the same mechanism as M2 receptors for para NS. Ach from vagus binds to M2 receptors which reduces cAMP. See notes for more details

31
Q

What is verapamil used to treat?

A

Reduction of ventricular responsiveness to atrial arrythmias
MOA
Depresses SA automaticity (by blocking the Ca channels in SAN) and subsequent AV node conduction

32
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

33
Q

What is amiodarone used to treat?

A

Supraventricular tachyarrhythmia

Ventricular tachyarrhythmia

34
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 (prolongs refractory)

35
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

36
Q

What is the target of cardiac glycosides like digoxin?

A

Na+/K+ ATPase

37
Q

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

A

twofold:
1. 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= inotropic effect

  1. central vagal stimulation causes increased refractory period and reduced rate of conduction through the AV node

Ie digoxin decreases the rate but improves the contraction = v good

38
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

39
Q

What is digoxin used to treat?

A

Atrial fibrillation

Atrial flutter

40
Q

What is an adverse effect of digoxin?

A

dysrhythmias (e.g. AV conduction block- blocking Na/K+ ATPase interferes with the gradients)

41
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)

42
Q

Which two beta blockers can be given to minimise the side effects of beta blockers like increased TPR

A

Drugs with ISA = eg pindolol. They can trigger some b2 mediated vasodilation and so the TPR wont rise as much

Drugs that are non selective between alpha and beta receptors: eg carvedilol. This is because alpha blockade can help with vasodilation

43
Q

side effects of amiodarone

A

Amiodarone accumulates in the body (t½ 10 - 100days)
Has a number of important adverse effects including:
- photosensitive skin rashes
- hypo- or hyper-thyroidism
- pulmonary fibrosis

Y2 LCRS Pharm Fwong (40 decks)

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