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Year 2 Pharma > Drugs and the heart > Flashcards

Drugs and the heart Flashcards

1
Q

What are the ‘funny’ channels in the heart? - I f channels

A

Hyperpolarization activated cyclic nucleotide gated channels - switch on during hyperpolarised states and utilise cyclic AMP and drive sodium entry to initiate depolarisation. On their own they do not produce enough to complete depolarissation, but it starts it

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2
Q

What is the predominant channel that drives depolarisation in Heart rate

A

Calcium channels - transient t type calcium channels or long lasting l type

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3
Q

What channels repolarise the cells controlling heart rate

A

-potassium channels

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4
Q

What is phase 4 in heart rate regulation

A

Spontaneous depolarization that triggers an action potential

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5
Q

Mechanism regulating heart contractility - describe the steps

A
  1. signal promotes calcium entry
  2. calcium activates RyR receptor
    - 25% of calcium comes from outside, 75% from sarcoplastic reticulum
  3. calcium promotes troponin binding and causing contraction
  4. repolarisation via sodium exchanging for calcium to export calcium out of cell and sodium potassium atpase maintains sodium levels in cell
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6
Q

What mechanisms increase the myocardial oxygen demand

A 
An increase in:
heart rate
preload
afterload
contractility
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7
Q

What are factors that can increase the myocardial oxygen supply

A

Increase in:
Coronary blood flow
Arterial O2 content

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8
Q

What drugs mainly effect rate of heart

A

Beta blockers and

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9
Q

What beta blockers effect on the heart rate

A

Sympathetic NS increases nodal activity, and therefore affects funny current and ca2+ channels
Therefore a beta blocker will stop the sympathetic NS therefore decrease If and Ica

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10
Q

Calcium antagonist effect on heart rate

A

Block Ca2+ therefore slow heart down

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11
Q

What affect ivabradine on heart rate

A

Block funny current therefore decreasing heart rate as spacing out the time between each depolarisation starting

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12
Q

What affect beta blockers and calcium channel blockers on contractility

A

decrease calcium entry therefore decrease contractility

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13
Q

What are the different types of calcium antagonists

A

there are two classes - rate slowing that have cardiac and smooth muscle actions and non rate slowing that only have smooth muscle actions, but these are more potent

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14
Q

What are examples of rate slowing drugs

A

Phenylalkylamines eg verapamil

Benzothiazepines eg diltiazem

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15
Q

What are examples of non rate slowing drugs

A

Dihydropyridines eg amlodipine

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16
Q

What effect do organic nitrates and potassium channel openers have on the heart and how does it do this?

A

It increases cyclic GMP therefore causing smooth muscle relaxation and hyperpolarisation (due to potassium efflux) of the cells making it harder to contract. K+ channel openers mainly just cause potassium efflux causing hyperpolarisation of the cell

17
Q

What two different effects of nitrates and potassium channel openers influence preload and afterload? What is a consequence of this?

A

It causes vasodilation therefore decreasing afterload
Venodilate causing a decrease in preload
Therefore a decrease in myocardial oxygen demand

18
Q

What is a stable angina

A

A cardiac stitch where the heart doesn’t receive enough oxygen during exercise causing pain

19
Q

What is the first line treatment of a stable angina? What is the problem of this treatment

A

Beta blockers or calcium channel blocker by reducing HR and contractility but make it harder to exercise as less response to sympathetic stimuli and therefore less Ca2+ influx

20
Q

beta blocker side effects

A

It can worsen heart failure as it makes your tissues less able to match CO to tissue needs, which is already a problem in heart failure.
It also increases vascular resistance by blocking dilating of vessels. This will make HF even worse as have to work harder to push blood around the body
Also causes bradycardia, and if a patient has conduction problems then this will be even worse

21
Q

What are examples of beta blockers used on the heart

A

Pindolol - an equal affinity for beta1 and beta 2 receptors with intrinsic sympathetic activity
Carvediol that causes an alpha 1 blockade causing additional vasodilator properties (alpha 1, beta 1 and 2)

22
Q

What kind of patients can you NOT use beta blockers for and why

A

Asthmastics and diabetics
They block B2 receptors in lungs therefore make asthma attacks worse
It also interferes with liver control of glucose and masks hyperglycaemia effects

23
Q

What is a common side effect of beta blockers that really bothers patients

A

Cold extremities (also a worsening peripheral artery disease) due to a loss of beta 2 receptor mediated cutaneous vasodilation in extremities therefore no blood in extremities

24
Q

Side effects of calcium channel blocker

A

they are ‘safer’ than beta blockers but they can cause bradycardia and constipation (can affect people from taking a drug)

25
Q

What are side effects of dihydropyridines

A

Ankle oedema due to vasodilation meaning more blood in capillaries causing fluid coming out
Headache/flushing due to vasodilation
Palpitations due to reflex tachycardia due to vasodilation of vessels

26
Q

What are the different arrythmias simply classified between

A

Supreventricular - above the ventricles
Ventricular
Complex ( a mix of both supra and ventricular)

27
Q

What is the vaughn williams classification

A

A classification of anti arrhythmic drugs: seperating the drugs into:
Class 1- sodium channel blockers
Class 2 - beta adrenergic blockade
Class 3 - prologation of repolarisation (membrane stabilisation mainly due to potassium channel blockade)
Class 4 - calcium channel blockade

28
Q

What drugs are used to treat supraventricular arrythmias and how does it do this?

A

Adenosine, binding to adenosine receptors having an inhibitory effect on adenylate cyclase and therefore inhibiting cyclic AMP therefore decrease funny current therefore reducing depolarisation via AV node
(less importantly also has effect on SM and promote relaxation)

29
Q

How does verapamil work

A

Block Ca2+ channels therefore decreasing ability to depolarisation therefore causing a longer time between the depolarisations therefore increases chances of normal rhythm starting

30
Q

How does amiderone work

A

Blocks re-entry arrhythmias

This is done by a potassium channel blockade therefore prolonging the repolarisation state

31
Q

What is a reentry rhythm

A

Where areas of damaged or dead tissue due to heart attack etc that causes a signal for a heart to contract coming back up the heart to cause a contraction instead of going as it would do, down the heart and cause contraction down the heart

32
Q

What are the effects of digoxin/.

A

Decrease stroke risk by inhibiting the Na K ATPase pump
Digoxin also increases refractory period and reduces rate of conduction through the AV node, therefore more time between heart contractions

33
Q

What effect does digoxin have on inotropy

A

Blocks Na K ATPase therefore blocking Na+ movement into the cell. This means that Na+ can’t be exchanged for Ca2+ successfully therefore more Ca2+ in cardiac muscle as it can’t move out. Therefore making cardiac muscle contractions more powerful.

34
Q

When is digoxin used

A

In AF and Atrial flutter particularly when worry about stroke

35
Q

Side effects of digoxin

A

Dysrhythmias due to AV conduction block

36
Q

What can make digoxin toxicity threshold worse therefore make effects worse and why

A

Hypokalaemias eg due to diuretic use due the digoxin binding to the potassium binding site. Potassium competes with digoxin for this site, and if K+ levels decrease then more digoxin binds to the target so has a more powerful effect

Year 2 Pharma (34 decks)

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