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Pharm OTL > Heart Drugs > Flashcards

Heart Drugs Flashcards

1
Q

Name three examples of ACE inhibitors

A

Ramipril
Lisinopril
Captopril
Perindopril

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2
Q

What is the MoA of ACEIs?

A

Inhibits angiotensin converting enzyme to reduce the production of angiotensin II.

This causes reduced vasoconstriction, reduced aldosterone secretion and reduced ADH release

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3
Q

State two conditions in which ACEIs are used

A

Hypertension

Heart failure

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4
Q

State three side effects of ACEIs

A

Dizziness
Dry cough
Hyperkalaemia
Renal failure

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5
Q

Name two ARBs

A

Candesartan
Losartan
Valsartan

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6
Q

What is the MoA of ARBs?

A

Blocks the AT1 (and AT2 but this is less important) receptors.

This causes vasodilation, reduced aldosterone secretion and reduced ADH release.

ACE is still working so bradykinin is still being broken down, therefore pts dont get a dry cough side effect.

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7
Q

State three side effects of ARBs

A

Hyperkalaemia
Renal failure
Dizziness

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8
Q

State two conditions in which ARBs are used

A

Hypertension

Heart faillure

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9
Q

Name two dihydropyridine CCBs

A

Amlodipine
Lercandidipine
Nifedipine

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10
Q

Name a phenylalkamine CCB

A

Verapamil

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11
Q

Name a benzothiazapine CCB

A

Diltiazem

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12
Q

State two conditions in which verapamil and diltiazem are used

A

Hypertension
Arrhythmias - supraV tachycardia, AV nodal re-entry
Angina

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13
Q

What is the MoA of verapamil and diltiazem?

A

Blocks L-type Ca2+ channels on myocytes - negative inotropy.

Slows SAN firing, and slows the conduction of the AVN - negative chronotropy.

Blocks L-type Ca2+ channels on vascular smooth muscle cells - reduced TPR.

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14
Q

State two side-effects of verapamil

A

Constipation
Bradycardia (therefore don’t use with beta-blockers)
Flushing

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15
Q

State two side-effects of diltiazem

A

Constipation
Skin reactions
Flushing

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16
Q

State two conditions in which dihydropyridine CCBs are used

A

Hypertension

Angina

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17
Q

What is the MoA of dihydropyridine CCBs?

A

Blocks L-type Ca2+ channels on vascular smooth muscle cells - reduced TPR

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18
Q

State two side-effects of dihydropyridine CCBs

A

Constipation
Peripheral oedema
Flushing
Headache

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19
Q

Name an alpha-adrenoceptor blocker

A

Doxazosin

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20
Q

What is the mechanism of action of alpha-adrenoceptor blockers?

A

Antagonises noradrenaline at post-synaptic alpha-1 receptors on smooth muscle cells of the vasculature.

Causes vasodilation.

Also reduces plasma LDL and TG levels, while increasing HDL levels.

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21
Q

State two conditions in which alpha-adrenoceptor blockers are used

A

Hypertension

BPH

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22
Q

State two side-effects of alpha-adrenoceptor blockers

A 
Postural hypotension
Headache
Oedema (especially with dihydropyridine CCBs)
Palpitations
Cystitis
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23
Q

Name two beta-blockers

A 
Bisoprolol
Carvedilol
Nebivolol
Metoprolol
Labetolol (used in pregnancy)
24
Q

Name two conditions in which beta-blockers are used

A
  • Hypertension
  • Angina
  • Heart faliure
  • Arrhythmias: SVTs, and converts AV nodal re-entry and WPW, protects ventricles from high rates of contraction
  • Anxiety
25
Q

What is the MoA of beta-blockers?

A

Decreased slope of the pacemaker potential at the SAN, and slowed conduction at the AVN - negative chronotropy

26
Q

State two side-effects of beta-blockers

A

Bradycardia (caution in diabetics - mask hypoglycaemic tachycardia)

Lethargy and impaired concentration

Erectile dysfunction

Bronchoconstriction (caution in asthmatics)

27
Q

What is the MoA of digoxin (cardiac glycoside)?

A

Increased vagal activity => slower heart rate.

Blocks the Na/K pump to increases intracellular Na+, which reduces the action of the NCX channel therefore more Ca2+ stays in the sarcoplasm to be released on contraction - increased inotropy.

28
Q

State two condtions in which digoxin is used

A

Heart failure

Arrhythmias - slows ventricular rates in SVT

29
Q

What is the MoA of ivabradine in heart failure and sinus tachycardia?

A

Slows the funny current to slow the heart rate

30
Q

What is the MoA of hydralazine and nitrate combination in heart failure?

A

Balanced ateriodilation and venodilation to reduce the pre-load and after-load on the heart

31
Q

Name a class IA antiarrhythmic

A

Procainamide

Quinidine

32
Q

What effects do class IA antiarrhythmics have on the ventricular action potential?

A

Prolongs the AP by:

  • Reducing Na+ conduction, therefore slowing the upstroke
  • Prolonging the refractory period
33
Q

State a use of class IA antiarrhythmics

A

Acute IV treatment of supraV and V tachycardias

34
Q

State a side effect of class IA antiarrhythmics

A

Torsades de Pointes (prolonged QT)
Lupus-like effects
GI effects
Hypotension

35
Q

Name a class IB antiarrhythmic

A

Lidocaine

Mexiletine

36
Q

What is the MoA of class IB antiarrhythmics?

A

Fast binding offset kinetics

37
Q

State a condition when class IB antiarrhythmics can be used

A

V tachycardia

38
Q

State a side effect of class IB antiarrhythmics

A

Dizziness
GI effects
Drowsiness

39
Q

Name a class IC antiarrhythmic

A

Flecainide

Propafenone

40
Q

What is the MoA of class IC antiarrhythmics

A

Slow binding offset kinetics leads to a longer AP duration by:

  • Slow upstroke
  • Increased refractory period
41
Q

State two conditions in which class IC antiarrhythmics can be used

A
  • SupraV arrhythmias - atrial flutter and fib
  • Premature ventricular contractions
  • WPWS
42
Q

State two side effects of class IC antiarrhythmics

A
  • Sudden death (with chronic use)
  • Proarrhythmic
  • Increased response of the ventricles to atrial flutter leading to raised HR (therefore can prescribe with bisoprolol)
  • Dizziness
  • Diplopia and blurred vision
43
Q

Name two class III antiarrhythmics

A 
Amiodarone
Sotalol (class II and III effects)
44
Q

What is the MoA of class III antiarrhythmics?

A

Block K+ channels to prolong the AP by:

  • Increasing the AP duration (longer plateau)
  • Increasing absolute refractory period

Also slows AV conduction

45
Q

Amiodarone can be used for most arrhythmias. However state two side effects of this drug

A

All increase with time:

  • Pulmonary fibrosis
  • Hepatic injury
  • Increased LDL cholesterol
  • Thyroid disease
  • Optic neuritis

Half life of 3mths

46
Q

What is the class II effect of sotalol?

A

Increases the time between APs to slow the HR

47
Q

State a side effect of sotalol

A

Insomnia
Proarrhythmic
Fatigue

48
Q

Name the two class IV antarrhythmics

A

Verapamil
Diltiazem
(Rate-limiting CCBs)

49
Q

What is the MoA of adenosine?

A

Give as a rapid IV bolus bc the half-life is only seconds

Binds to Adenosine 1 receptors and activates K+ currents at the SA and AV nodes.

Causes hyperpolarisation

Adadenosine

50
Q

State a use of adenosine

A

Convert re-entrant supraV tachycardias e.g. WPW, AVRT (not AF)
Slow the heart rate when doing an ECG to see SVTs more clearly
Diagnose coronary artery disease

51
Q

When is atropine used?

A

Symptomatic vagal bradycardia as atropine is a muscarinic antagonist

Matropine

52
Q

What is the aim of treatment for SVTs?

A

Rate control:

  • Bisoprolol *
  • Verapamil *
  • Diltiazem *
  • Digoxin

Rhythm control:

  • Sotalol
  • Flecanide with bisoprolol *
  • Amiodarone
  • Commonly used
53
Q

Which drugs are commonly used in WPW?

A

Flecainide and amiodarone

54
Q

Which drugs are commonly used in VT?

A

Metoprolol/ bisoprolol
Mexiletine
Amiodarone

55
Q

How do anti-arrhythmics compare to one another in terms of safety and tolerability?

A

Safe:

  • Bisoprolol
  • Verapamil and diltiazem

Increased risk:

  • Sotalol
  • Flecainide
  • Mexiletine
High risk (but most effective):
- Amiodarone

Pharm OTL (18 decks)

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