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Year 2 LCRS Pharmacology > 11: Drugs of the Heart > Flashcards

11: Drugs of the Heart Flashcards

1
Q

Explain the channels involved in evoktion of an cardiac pacemaker cell potential

A
  1. If: Hyperpolarization-activated cyclic nucleotide–gated channels (HCN) (mediated via cAMP): If –> Funny- Chanels (spontaneous depolerisation via Kation influx)
  2. ICa(t): Transeient Ca2+ channels (open due to K+ influx)
  3. ICa(L): Long-Lasting Ca2+ channels
  4. IK: K+ Channels –> cause depolerisation
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2
Q

Which factors influence Heart contractility?

A

Mainly Calcium Levels, which are influenced by:

  1. Ca2+ influx via the L-type calcium channels due to depolerisation (25%)
  2. Ca2+ induced Ca2+ release from the SR vie the Ryanodine receptor (RyR) (75%)
  3. Calcium transport out of the cell
    • Na+/Ca2+ exchanger
    • –> Na+/K+ ATPase (influences Na+ levels, thereby influences Ca2+ levels)
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3
Q

What is the influence of the SNS on the Cardiac pacemaker potential?

A
  1. Increase cAMP--> triggering of Ifto occur which causes an
  2. increase in ICa
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4
Q

What is the impact of the PNS on the cardiac pacemeker current?

A
  1. decrease of cAMP –> decrease If
  2. IK (K+) increase –> higher polarization
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5
Q

Which facctors influence myocardial oxygen supply?

A
  1. Arterial O2 levels
  2. Coronary blood flow (mainly used as drug target)
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6
Q

Which factors influence myocardial oxygen demand?

A
  1. Preload
  2. Afterload
  3. Contractility
  4. Heart Rate
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7
Q

What are the effects of ß-blockers on the heart?

What is their MOA?

A

MOA:

  • decrease cAMP which leads to a decrease in
    • If–> less depolerisation, leading to
    • decreased ICa

Causing

  • Reduced HR (negative chronotropy)
  • Reduced Contractility (negative inotropy)
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8
Q

What are the contraindications for administration of a ß-blocker?

Why?

A
  1. Heart failure
    • might worsen HF
      • even further decreased CO
      • increased TPR (blocking of ß2 mediated vasodilation)
  2. Astmah
    • Bronchospasm
  3. Heart block
    • Might cause Bradycardia if there is decreased conduction at AV node
  4. Diabetis
    • might mask symptoms of Hypoglycaemia
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9
Q

What are the common side effects of ß-blockers?

A
  1. Bradycardia
  2. Bronchospasm
  3. Cold extremities
  4. (Hypoglycaemia)
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10
Q

How could you overcome the negative effects of ß-blockers in Heart Failure and still use it as an effective treatment?

A
  1. Chose ß-blockers with ISA (e.g. Pindolol)
  2. Mixed alpha+ ß blockers –> a1 blocker gived additional vasodilation –> no problem with vasoconstriction (e..g Carvedilol)
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11
Q

What types of Calacium-Channel blockers are there?

A

Calcium anatgonists can be

  1. Rate slowing​​ (e.g. Phenylalkylamines (e.g. Verapamil), Benzothiazepines (e.g. Diltiazem)
    • ​​​​​Caridiac and SM actions
  2. Non-rate slowing (Dihydropyridines (e.g. amlodipine))
    • ​​only SM actions
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12
Q

What is the MOA of Calcium channel antagonists?

What is the effect?

A
  1. Decrease ICa
    • ​​less intracellular Ca
      • reduced contractility
      • reduced HR (slower depolerisation hence activation of IK)
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13
Q

Which Drugs are classified as Rate slowing Ca2+ channel antagonists?

A
  1. Phenylalkamines (e.g. Verapamil)
  2. Bezothiazepines (e.g. Diltiazem)
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14
Q

Which Drugs are classified as non-rate slowing Calcium channel blockers?

A

Dihydropyridines (e.g. amlodipine)

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15
Q

What are the side effects of the use of Verapamil?

A

Vermapril= Rate slowing CCB can lead to

  • Bradicardia and AV block (due to Ca2+ block)
  • Constipation (block of Ca2+ channles in gut)
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16
Q

What are the side effects of the use of Dihydropyridines?

A

Dihydropyridine= Non-rate slowing Calcium-Channel-Blocker (CCB)

  • Strong Vasodilatory effects that might lead to
    • ankle oedema (due to increased pressure in capillaries with increased blood)
    • headaches, flushing (vasodilation in head)
    • Palpitations (due to reflex tachicardia)
17
Q

What is the MOA of the use of organic nitrates in the treatment of Angina?

What are the effects?

A
  1. NO increases the activity of Guanylyl cyclase
  2. Leads to an increase of cGMP
  3. Causes SM relaxation
    • ​​directly
    • via K+ channel opeining causeingh hyperpolerisation

Leading to

  1. an increase in Coronary blood flow
  2. reduction in Pre+Afterload –> reduction in myocardial oxygen demand
18
Q

What is the MOA of the use of K+channel openers in the treatment of Angina?

What are the effects?

A

Hyperpolerisation of the cell –> decreased Ca2+ influx

–> relaxation

19
Q

How would you treat Angina?

A
  1. Either ß-blocker or CCB
  2. Switch if drug of 1 is not well tolerated
  3. Combine ß-blocker + CCB
  4. If both are not tolerated consider
    • nitrates
    • Ivabriandin (If inihibitor)
20
Q

What are the aims of treatement of Arrythmias?

A
  1. To reduce sudden death
  2. To decrease the risk of stroke
  3. To alleviate symptoms
21
Q

What is the Vaughan-Williams Classification?

A

It is a way of classifiing Anti-arrythmic drugs

22
Q

Recall the Vaughan-Williams-Classification of anti-arrythmic drugs

A

There are 4 types of drugs:

  1. Sodium Channel blocker
  2. ß-blocker
  3. Prolongation of repolerisation (membrane stabelising drugs), mainly due to K+ blocker
  4. CCB
23
Q

What are the limitations of the Vaughan-Williams Classification of anti-arrythmic drugs

A

It was developed when

  1. little number of drugs were known
  2. Mechanisms were not known too well

–> Now:

  • Mechanisms of drugs are better understood–> many drugs have several effects and can fit into more than 1 class –> no clear classification possible
24
Q

What is the ending most ACE inhibitors end on?

25
Which drugs whould you use for treatment of Supraventricular Arrythmias?
1. Adenosine 2. Verapamil
26
Explain the MOA, effect and use of Adenosine
It is used in the Treatment of Supraventricular tachy-arrythmias 1. Binds to Adenosine Receptors on 1. SA node--\> reduced cAMP --\> reduction in If and therefore **rate-slowing** 2. Smooth muscle --\> SM relaxation --\> **decrease in TPR** Due to its short t1/2 (30s) --\> mainly used in IV hospital settings (safe due to short t1/2)
27
Explain the connection between HR controll and controll of arrythmias
In many arrythmias (expecially supraventricular) there is an irregular contraction of muscle When HR is slowed--\> there is the hope for more regular/ more controlled contraction of muscle leading (hopefully) to a longer filling phase and better ejection
28
What is the MOA and effect of Verapamil?
Verapamil= Supraventricular anti-arrythmic CCB MOA: * Depresses SA automaticity and subsequent AV node conduction Effect: * Reduction of ventricular responsiveness to atrial arrythmias
29
What is the MOA of Digoxin
VIa 2 Mechanisms: 1. **Binds to Na+/K+ pumps (inhibitory)** 2. Higher intracellular Na+ 3. Slows down Na+/Ca2+ exchanger --\> less Ca2+ transport out of the cell 1. **Increase in Intracellular Ca2+** 2. **Increase in contractility** * **Vagal activation**--\> causes increased refractory period and reduced rate of conduction through the AV node
30
Why is hypokalaemia a contraindication of digoxin?
Digoxin compedes with K+ on the K+/Na+ATPase --\> in hypokalaemia --\> risk of toxic dose becasue it is more effective Risk of Heart Block
31
Name a cardiac glycoside
e.g. Digoxin
32
What are the indication for use of Digoxin? Why?
Normally used in AF/arteriral Flutter with begining signs of Heart Failure because of 1. positive inotropic effect 2. with rate slowing effect (AV-conductance reduced) --\> less beats are conducted onto the atria
33
What are the side-effects of Digoxine?
•dysrhythmias (e.g. AV conduction block, ectopic pacemaker activity) --\> Beware Hypercalcaemia (risk of digitalis toxicity); hypokalaemia (risk of digitalis toxicity)! (drug is more effective)
34
What is Reentry arrythmia?
A form of arrythmia that is caused by occurance of an additional way of conductance (e.g. due to damage to fibres that block out the option for neutralising a potential) (Reentry shown in blue) that triggers a second contraction/potential of a single pacemaker potential
35
What are the indication for use of Amiodarone?
•superventricular and ventricular tachyarrhythmias – often due to **reentry**
36
What is Amiodarone?
A drug used in the treatment of arrythmias (• Complex action probably involving multiple ion channel block)
37
What is the effect and MOA of Amiodarone?
• Complex action probably involving multiple ion channel block leading to a prolonged repolerisation--\> new potential is generated later
38
What are the side-effects of Amiodarone?
* Long t1/2--\> accumulation in the body (t½ 10 - 100days) whith chronic intake (not really safe to take) * photosensitive skin rashes * hypo- or hyper-thyroidism * pulmonary fibrosis

Year 2 LCRS Pharmacology (38 decks)

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