Drugs & CVS Flashcards

1
Q

What are the 4 classifications of anti-arrhythmic drugs?

A
  1. Class 1 : drugs that block voltage sensitive sodium channels
  2. Class 11 : antagonists of beta-adrenoreceptors
  3. Class 111: drugs that block potassium channels
  4. Class 1V: drugs that block calcium channels
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2
Q

Give an example of a class 1 drug

A

Lidocaine

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3
Q

Explain how a class 1 drug works eg lidocaine

A

Loclass 1 drugs blocks voltage gated Na+ channels in open or inactive state.

Damaged myocardium can spontaneously depolarise causing arrhythmia’s eg AF. Lidocaine works in this condition by blocking Na+ channels after an action potential , therefore preventing the initiation of another action potential.

Sometimes used after an MI. INTRAVENOUSLY

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4
Q

Give examples of class 11 drugs

A

Propranolol , atenolol ( BETA BLOCKERS j

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5
Q

Outline the mechanism of action of class || drugs

A
  1. They block the sympathetic action by blocking B1 receptors in the heart to slow the heart rate ( negative chronotropy).
  2. Blocking the b1- receptors causes a reduced heart rate due to a decreased slope of the pacemaker potential in the SA node as the SA nodes increases the time taken to initiate an action potential
  3. AND slows conduction in the AV node to increase the time between depolarisation of the atria and the ventricles.
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6
Q

When are beta blockers used ?

A
  1. Used following an MI. This is because MI often causes increased sympathetic activity and arrhythmia may be partly due to the increased sympathetic activity. Beta blockers prevent ventricular arrythmias.
  2. Can prevent supraventricular tachycardia as beta blockers slow conduction in the AV node. It also slows ventricular rate in patients with AF.
  3. Reduce myocardial ischaemia by reducing oxygen demand.
  4. In heart failure
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7
Q

Give an example of a class ||| drug

A

Amiodarone

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8
Q

Outline the mechanism of action of class 111 drugs

A

They block potassium channels which prolongs the action potential and lengthens the absolute refractory period to slow the heart rate down. This prevents another action potential from forming. However , these drugs can actually be pro-arrhythmic as they promote early after depolarisations.

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9
Q

Why is amiodarone considered a good class 111 drug ?

A

Because it has other actions in addition to blocking K+ channels for example it is also a beta blocker and calcium channel blocker.

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10
Q

When do we use class 111 drugs ?

A
  1. Can be used to treat most arrhythmias , however it is not first line in most cases due to side effects .
  2. Treat tachycardia associated with Wolff-Parkinson white syndrome.
  3. Suppress ventricular arrhythmias post MI.
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11
Q

Give examples of class 1V drugs ?

A

Verapamil ( act on the heart to give negative chronotropic and inotropic effects )

Diltiazem ( act on the heart to give negative inotropic and chronotropic effects )

Dihydropyridine eg Amlodipine which work on smooth muscle vasculature by promoting systemic vasodilation. These are NOT effective in preventing arrhythmias.

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12
Q

What is the mechanism of action of class 1V drugs ?

A
  1. Can act on the myocardium to decrease the slope of the action potential at the SA node and decrease AV node conduction by blocking calcium channels
    This leads to negative inotropic and negative chronotropic effects.
  2. Class 1V drugs can also block calcium channels on smooth muscle cells to reduce contraction. This leads to the dilation of blood vessels to reduce total peripheral resistance. Which then decreases arterial blood pressure. And reduces the workload of the heart by reducing afterload.
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13
Q

What is Adenosine ? And what is its importance

A

An endogenous substance that is produced in our body in small amounts at psychological levels.

It can be given IV which acts on a1 receptors to enhance potassium conductance and hyperpolarised cells. This hyperpolarisation inhibits the movement fo calcium and essentially re sets the SA node. It has a very short half life.

The patient will feel like their heart has stopped when adenosine is given.

It is important because it is an anti-arrhymic drug but does not belong to any of the classes. It is useful for terminating re entrant SVT.

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14
Q

What are ACE-inhibitors ( ACEi) ?

A

Very important in reducing hypertension and heart failure.

They inhibit the action of angiotensin converting enzyme. This , this would prevent the conversion of angiotensin 1 to angiotensin 11.

This is important because angiotensin 11 acts on the kidneys to increase Na+ and water reabsorption. Angiotensin 11 is also a vasoconstrictor. And angiotensin 11 also stimulates release of aldosterone from the adrenal cortex.

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15
Q

What are the common side effects on patients who take Angiotensin converting enzyme inhibitors ?

A

CNS cause a dry cough due to excess bradykinin building up in the lungs this is because ACE is used to break down bradykinin but now that it is inhibited , bradykinin builds up.

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16
Q

Why are ACE-inhibitors important in the treatment of heart failure ?

A

,this is because ACEi decrease vasomotor tone which means they decrease blood pressure.

This reduces the afterload of the heart. And reduces pre load of the heart.

Both effects reduce the work load of the heart.

17
Q

In a patient who cannot toleratte ACEi eg due to build up of bradykinin , what is an alternative ?

A

Angiotensin 1 receptor blockers which block angiotensin 1 receptors which prevents angiotensin 11 from binding. This leads to a reduced effect of Angiotensin 11.

They have the same effect as ACEI but ACE enzyme is not affected so bradykinin can still be broken down.

18
Q

Ca2+ channel blockers are useful in which problems ?

A

Hypertension

Angina

Coronary artery spasm

Supraventricular tachycardia

19
Q

What are the two types of positive inotropic ?

A
  1. Cardiac glycosides

2. Beta-adrenergic agonists

20
Q

Give an example of cardiac glycosides

A

Digoxin

21
Q

Outline the mechanism of action of cardiac glycosides such as digoxin

A
  1. Blocks Na+/K+ ATPase
  2. This causes an increase in intracellular Na+
  3. This leads to a decrease in activity of the nA+/Ca2+ exchanger. Which leads to more Ca2+ stored in the SR.
  4. This leads to an increased force of contraction

IMPROVES SYMPTOMS IN PATIENTS WITH HEART FAILURE BUT NO LONG TERM ACTION

22
Q

Outline the action of cardiac glycosides on heart rate

A

Cardiac glycosides also cause increased a gala activity. This slows AV conduction and slows the heart rate.

May be used in heart failure when there is an arrythmia such as AF

23
Q

Give examples of beta-adrenoreceptors agonist

A

Dobutamine

24
Q

Summarise the way to treat heart failure.

A

Cardiac glycosides will relieve symptoms by making the heart contract harder , however there is no long term benefits as making the heart work harder is not good in the long run. It is better to reduce workload.

Therefore ACEi or ARB or diuretics are better for heart failure as they reduce the workload of the heart. Beta blockers can also reduce workload of the heart

25
Q

What is angina?

A

When o2 supply to the heart does not meet its demands. This is of a limited duration and does not result in death of myocytes.

When ischaemia of heart tissue occurs , chest pain arises.

26
Q

How can we treat angina ?

A

Organic nitrates

27
Q

What is the mechanism of action of nitrates ?

A
  1. Organic nitrates react with thiols ( SH) in vascular smooth muscle which causes NO2- fo be released.
  2. NO2- is reduced for NO ( nitric oxide )
  3. Nitric oxide is released endogenously from endothelial cells.
  4. Nitric oxide is most effective on VEINS - less of an effect on arteries
  5. Nitric oxide causes venodilation of veins.
  6. Venodilation of veins lowers pre load , which reduces work load of the heart. The heart fills less therefore force of contraction reduced. This lowers O2 demands.
28
Q

How does nitric oxide cause vasodilation ?

A

Nitric oxidie activates guanylate cyclase. This catalyses the formation of cGMP from GTP. CGMPthen goes off to activate protein kinase G.

Protein kinase G then works by lowering intracellular Ca2+

Which causes relaxation of vascular smooth muscle

29
Q

What heart conditions increase the risk of thrombus formation ?

A

AF

acute myocardial infarction

Mechanical prosthetic heart valves

30
Q

What drug is commonly given as an anti thrombotic drug to someone with AF ?

A

Warfarin ( orally) which antagonises the action of vitamin K

Direct oral thrombin inhibitors such as dabigatran are more commonly used now , where you don’t have to check their INR.

31
Q

How is heparin given usually ?

A

IV - it inhibits thrombin used acutely for short term action

Fractioned heparin is given using a subcutaneous injection.

32
Q

Give an example of an anti platlet drug

A

Aspirin

Clopidogrel

Used following acute MI or high risk MI