Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which facctors influence myocardial oxygen supply?

A
  1. Arterial O2 levels
  2. Coronary blood flow (mainly used as drug target)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which factors influence myocardial oxygen demand?

A
  1. Preload
  2. Afterload
  3. Contractility
  4. Heart Rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the common side effects of ß-blockers?

A
  1. Bradycardia
  2. Bronchospasm
  3. Cold extremities
  4. (Hypoglycaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A
  1. Phenylalkamines (e.g. Verapamil)
  2. Bezothiazepines (e.g. Diltiazem)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Dihydropyridines (e.g. amlodipine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

-pril

25
Q

Which drugs whould you use for treatment of Supraventricular Arrythmias?

A
  1. Adenosine
  2. Verapamil
26
Q

Explain the MOA, effect and use of Adenosine

A

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
Q

Explain the connection between HR controll and controll of arrythmias

A

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
Q

What is the MOA and effect of Verapamil?

A

Verapamil= Supraventricular anti-arrythmic

CCB

MOA:

  • Depresses SA automaticity and subsequent AV node conduction

Effect:

  • Reduction of ventricular responsiveness to atrial arrythmias
29
Q

What is the MOA of Digoxin

A

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
Q

Why is hypokalaemia a contraindication of digoxin?

A

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
Q

Name a cardiac glycoside

A

e.g. Digoxin

32
Q

What are the indication for use of Digoxin?

Why?

A

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
Q

What are the side-effects of Digoxine?

A

•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
Q

What is Reentry arrythmia?

A

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
Q

What are the indication for use of Amiodarone?

A

•superventricular and ventricular tachyarrhythmias – often due to reentry

36
Q

What is Amiodarone?

A

A drug used in the treatment of arrythmias (• Complex action probably involving multiple ion channel block)

37
Q

What is the effect and MOA of Amiodarone?

A

• Complex action probably involving multiple ion channel block

leading to a prolonged repolerisation–> new potential is generated later

38
Q

What are the side-effects of Amiodarone?

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions