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YR2 LCRS Pharm > 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

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

A

Dihydropyridine receptors

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3
Q

What happens to calcium once it has passed into the cell via dihydropyridine receptor channels?

A

It binds to ryanodine receptors on the SR + causes Ca2+ release from the SR

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4
Q

How does calcium stimulate contraction?

A

It binds to troponin on Actin

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5
Q

What are the different ways in which calcium is removed from the myoplasm after it has stimulated contraction?

A

Na+/Ca2+ exchanger

SERCA2a (sarcoendoplasmic reticulum calcium ATPase)

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6
Q

What features of contraction is SERCA2a responsible for and why?

A

Rate of calcium removal: thus rate of cardiac muscle relaxation
Size of calcium store: thus affects contractility of the subsequent beat

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7
Q

What are the 3 main channels that are responsible for the action potential in the sinoatrial node?

A

If channel: hyperpolarisation-activated cyclic nucleotide-gated (HCN) channel (funny channel)
Ca2+ channel (Transient + Long-lasting)
K+ channel

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8
Q

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

A

If channels open in hyperpolarised state, utilising cAMP, drive in Na+ to initiate depolarisation
Current starts to rise, stimulating the opening of Ca2+ channels (T then L), which further depolarises the membrane.
K+ channels are responsible for repolarisation

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9
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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10
Q

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

A

It is negatively coupled with adenylate cyclase, thus decreases cAMP + interferes with funny currents, slows HR
Promotes K+ channel opening

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11
Q

What are the determinants of myocardial oxygen supply?

A

Arterial oxygen content

Coronary blood flow

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12
Q

What are the determinants of myocardial oxygen demand (work)?

A

Heart rate
Contractility
Preload
Afterload

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13
Q

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

A

B-blockers decrease If + Ca2+ channel activity
Ca2+ channel blockers decrease Ca2+ channel activity
Thus both decrease HR + contractility

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14
Q

Name a drug that decreases If activity.

A

Ivabradine (blocks the If channel)

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15
Q

What effect does Ivabradine have on contractility?

A

No effect on contractility because it doesn’t affect the Ca2+ channels

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16
Q

What are the 2 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
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17
Q

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

A

Reflex tachycardia due to profound vasodilation

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18
Q

How do organic nitrates cause vasodilation?

A

Organic nitrates are substrates for NO production
NO diffuses into smooth muscle + causes relaxation by activating guanylate cyclase that produces cGMP
cGMP also causes opening of K+ channels + K+ efflux, resulting in hyperpolarisation

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19
Q

How do potassium channel openers work?

A

They open K+ channels + hyperpolarise the smooth muscle so it is less likely to contract

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20
Q

How do vasodilation and venodilation reduce myocardial oxygen demand?

A

Reduce pressure against which the heart is pumping (reduce afterload)
Reduce venous return to the heart (reduce preload)

21
Q

State 5 unwanted effects of beta-blockers.

A 
Bradycardia  
Hypotension  
Hypoglycaemia in diabetics on insulin  
Cold extremities (loss of beta-2 receptor mediated cutaneous vasodilation) 
Bronchoconstriction
22
Q

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

A

Heart failure (CO already reduced)
B-Blockers further reduce CO + increase vascular resistance (B2 receptors are dilating receptors, so less vasodilation occurs)
Asthmatics: B2 blockade in lungs worsens attacks
Diabetics: Hypoglycaemia masked

23
Q

What are the side effects of verapamil?

A

Bradycardia + AV block (Ca2+ channel block)

Constipation (Gut Ca2+ channel block)

24
Q

What are the side effects of dihydropyridines?

A

Ankle oedema (vasodilation increases pressure on capillary vessels)
Headaches/flushing (vasodilation)
Palpitations (reflex sympathetic response)

25
Q

What is a simple classification of arrhythmias based on?

A

Point of origin

Supraventricular, Ventricular + Complex

26
Q

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

A 
Vaughan-Williams classification 
I: Na+ channel blockers  
II: B-blockers  
III: prolongation of repolarisation (mainly due to K+ channel blockade) 
IV: Ca2+ channel blockers
27
Q

What is adenosine used to treat?

A 
To terminate supraventricular tachyarrhythmias
Short lived (20-30s), thus quite safe
28
Q

How does adenosine work?

A

Binds to A1 receptors on nodal cells
Inhibitory effect on adenylate cyclase, inhibits cAMP production + funny currents, reduces depolarisation (tissue has longer time to repolarise)
Binds to A2 receptors on vascular smooth muscle
Increases cAMP, promotes relaxation + vasodilation

29
Q

What is verapamil used to treat?

A

Supraventricular arrythmias

30
Q

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

A

L-type calcium channel

Reducing Ca2+ entry means speed with which the tissue depolarises is reduced

31
Q

What is amiodarone used to treat?

A

Supraventricular tachyarrhythmia

Ventricular tachyarrhythmia

32
Q

How does amiodarone work?

A

By blocking many ion channels
Main effect through K+ channel blockade
This prolongs repolarisation, thus prolonging the time during which the tissue can’t depolarise

33
Q

Describe re-entry.

A

In damaged cardiac tissue signal passes down 1 branch of conductive tissue, but can’t pass down another. When signal passes through a third branch (usually the 2 signals would meet + cancel out) the signal goes back up 2nd branch + reactivates the tissue
Causes premature contraction (if muscle in ready state)

34
Q

What is the target of cardiac glycosides like digoxin?

A

Na+/K+ ATPase

35
Q

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

A

Blockage of Na+/K+ ATPase causes accumulation of Na+ in the cell
Excess Na+ is then removed by Na+/Ca2+ exchanger, thus increasing the intracellular Ca2+ concentration
Causes inotropic effect (increases force of contraction)
Also causes vagal stimulation which increases refractory period + reduces rate of contraction through AVN

36
Q

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

A

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

37
Q

What is digoxin used to treat?

A

Atrial fibrillation

Atrial flutter

38
Q

What is an adverse effect of digoxin?

A

Dysrrhythmia

39
Q

What effect does the sympathetic system have on SA nodal cells?

A

Increases cAMP, increases opening of If + Ca2+ channels
Increased chance of depolarisation
Increased HR

40
Q

Why is afterload a determinant of myocardial oxygen demand?

A

The higher the afterload, the harder the heart has to contract to eject blood from the heart

41
Q

Why is preload a determinant of myocardial oxygen demand?

A

Due to Starlings law

If increased volume returned to heart, heart will have higher stroke volume + have to work harder

42
Q

How do B blockers help decrease heart rate in angina?

A

Sympathetic nervous system exerts its effects via B1 receptors in heart
Blockade stops sympathetic stimulation, so stops the opening of If + Ca2+ channels

43
Q

What B blocker may be appropriate to use in heart failure patients with angina and why?

A

Pindolol
Has intrinsic sympathetic activity at low sympathetic levels
Thus in normal daily life it helps HF
B blockade prevents pain during exercise

44
Q

Why should B-blocker usage in heart block patients or those with conduction problems be avoided?

A

B-blockers cause bradycardia, exacerbating decreased conduction through AVN

45
Q

Which B blocker drugs can be used to attempt to prevent increased vascular resistance?

A

Mixed A-B- Blockers

Alpha blockade causes more dilation than constriction

46
Q

Name 2 types of arrhythmia

A

Bradyarrthmia (decreased HR)

Tachyarrythmia (increased HR)

47
Q

Why must Amiodarone be used with caution?

A

It accumulates in the body

Serious side effects (photosensitive skin rashes, hypo/ hyperthyroidism, pulmonary fibrosis)

48
Q

Why must potassium levels be monitored after digoxin administration?

A

Hypokalaemia lowers threshold for digoxin toxicity
Digoxin binds to same site as K+
So if blood K+ falls, digoxin has easier access to target + more powerful effect
Side effects increase

YR2 LCRS Pharm (34 decks)

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