Brainscape's Knowledge GenomeTM

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


See full index

LCRS 1 - Pharmacology > Drugs and the heart > Flashcards

Drugs and the heart Flashcards

1
Q

How are heart rate and contractility regulated?

A

SERCA2a is responsible for the removal of >70% myoplasmic Ca

Tf SERCA2a determines:

  1. Rate of Ca removal - tf rate of cardiac muscle relaxation
  2. Size of Ca store - tf cardiac contractility in subsequent beat

SERCA2a activity is regulated by interaction with phospholamban (PLN):

  • Dephosphorylated PLN INHIBITS SERCA2a
  • Phosphorylated by PKA, PLN dissociates from SERCA2a activating Ca pump –> increases rate of cardiac relaxation –> increases contractility in proportion to elevation in size of SR Ca store and the resulting increase in Ca release from SR
  • PLN is dephosphorylated by protein phosphatase (PP1) - terminates stimulation phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which drugs impact heart rate and contractility and how?

A
  1. Beta blockers - If + Ica - impact both
  2. Calcium channel antagonists - Ica - impact both
  3. Ivabradine - If - impacts HR

Beta blockers:
Block beta receptors –> less cAMP produced –> less downstream signalling to promote cardiac contractility

CCAs:
Block Ica in plasma membrane –> reduced influx of external Ca –> reduced Ca release from SR

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

Which drugs impact myocardial oxygen supply?

A
  1. Organic nitrates

2. Potassium channel openers

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

What are the different classes of calcium channel antagonists?

A

Rate slowing

  • Phenylalkylamines, e.g. verapamil
  • Benzothiazpeines, e.g. diltizaem

Non-rate slowing
- Dihydropyridines, e.g. amplodipine

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

What are the side effects of beta blockers?

A

Despite being cardioselective, most drugs have some b2 effects as well:

  1. Worsening of cardiac failure
  2. Bradycardia (heart block) - due to less conduction thr AVN
  3. Bronchoconstriction - b2 blockade in airways
  4. Hypoglycaemia - in diabetics on insulin, decreased glycogenolysis/gluconeogenesis
  5. Cold extremities + worsening of peripheral arterial disease - b2 blockade in skeletal muscle vessels

Possible - fatigue, impotence, depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is myocardial oxygen supply regulated?

A

Coronary vessels deliver O2 and nutrients to heart muscle depending on how hard heart is working, which depends on:
HR, preload, afterload, contractility

Increased venous return –> increased preload –> increased contractility

Increased TPR –> increased afterload –> heart must work harder against increased TPR

All associated with increased myocardial work and myocardial O2 demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the Vaughan Williams classification?

A

Classifies anti-arrhythmic drugs by mechanism of action

I - Na channel blockade
II - Beta adrenergic blockade
III - Prolongation of repolarisation (membrane stabilisation, mainly due to K channel blockade)
IV - Ca channel blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the major side effects of non-rate slowing CCAs (DHPs)?

A

Reflex tachycardia

Bc they have no effect on the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What effect do rate slowing CCAs have on the CVS?

A

Reduce HR

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do drugs affect myocardial oxygen supply and demand?

A

Vasodilation reduces TPR tf reduces afterload
Heart has to work less hard against resistance

Venodilation –> reduces venous return –> reduces preload + contractility

Reduced afterload + preload –> reduced myocardial oxygen demand

Improves balance between supply and demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do K channel openers work to reduce myocardial oxygen demand?

A
  • Promote K efflux to hyperpolarise the smooth muscle
  • Reduce ability to contract
  • Promotes smooth muscle relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do organic nitrates work to reduce myocardial oxygen demand?

A

Promote NO production in endothelial cells
NO diffuses into VSM
Vasodilation of coronary vessels and relaxation by activating guanylate cyclase
Promote smooth muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What drugs are used to treat angina?

A
  1. Beta blocker
  2. Organic nitrates
  3. K+ channel openers
  4. CCAs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the side effects of CCAs?

A

CCAs that target heart (rate-limiting) have similar side effects to beta blockers - verapamil

  1. Bradycardia, AV block, HF (Ca channel block)
  2. Constipation (gut Ca channels)

DHPs

  1. Fluid accumulation - ankle oedema
  2. Headache/flushing - vasodilation
  3. Palpitations
  4. Reflex tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the limitations of the Vaughn Williams classification?

A

Too many drugs cross classes

Limited clinical significance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do CCAs treat angina?

A
  • Bind to and inhibit opening of L-type calcium channels
  • Rate-slowing CCAs (verapamil, diltiazem) have effects on heart + BVs
  • Non-RS CCAs (DHPs, e.g. amlodipine)
    act mainly on BVs
  • All CCAs cause arterial vasodilation and reduce cardiac workload by this mechanism
  • Verapamil also has negative inotropic and chronotropic actions as a result of reducing Ca2+ entry into cardiac myocytes
17
Q

What are the side effects of organic nitrates?

A
  • Hypotension

- Headache

18
Q

What agents are used to treat arrhythmias?

A
  1. Adenosine
  2. Rate-slowing CCA (verapamil)
  3. Amiodarone
  4. Digoxin and cardiac glycosides
19
Q

Why is amiodarone used in the treatment of arrhythmias?

A
  • Prolongs repolarisation by multiple ion channel blockade (mainly K)
  • Prolongs time during which heart cannot depolarise, thus restoring normal rhythm
  • Reduces re-entry
20
Q

What are the adverse effects of amiodarone?

A
  • Long-lasting effects and long half-life tf accumulates in the body
  • Important adverse effects on the skin, lungs and thyroid
21
Q

Why is adenosine used in the treatment of arrhythmias?

A
  • Endogenous mediator produced by the metabolism of ATP
  • Acts on a1 receptors to hyperpolarize cardiac tissue and slow conduction through AVN
  • i.v. to terminate superventricular tachyarrhythmias (SVT)
22
Q

Why are digoxin and cardiac glycosides used in the treatment of arrhythmias?

A
  • Inhibitors of Na-K ATPase (Na/K pump)
  1. Cardiac slowing and reduced rate of conduction through AVN (largely as a result of central vagal stimulation)
  2. Increased force of contraction
23
Q

What drugs can be used to treat acute HF after cardiac surgery or in cardiogenic or septic shock and why?

A
  1. b1 adrenoceptor agonist (dobutamine)
    - Stimulates cardiac contraction
    - Doesn’t have too marked an effect on HR
  2. Glucagon - endogenous peptide hormone
24
Q

What are the side effects of digoxin?

A

Dysrrhythmias (e.g. AV conduction block, ectopic pacemaker activity)

LCRS 1 - Pharmacology (33 decks)

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