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Pharm Y2S1 > Cardiology Drugs > Flashcards

Cardiology Drugs Flashcards

1
Q

Give examples of the functional responses of alpha-1 adrenoceptors.

A

Vasoconstriction
Increased blood pressure
Contraction of visceral smooth muscle
Relaxation of GI tract

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2
Q

What is adrenaline used for in clinical practice?

A

Adjunct in cardiopulmonary resuscitation
In anaphylaxis
To extend effects of local anaesthesia

All effects are due to vasoconstriction and increasing blood pressure, promotes blood flow to coronary and cerebral arteries

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3
Q

Give examples of alpha-1 adrenoceptor agonists.

A

Phenylephrine, methoxamine, adrenaline, noradrenaline

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4
Q

Give examples of alpha-2 adrenoceptor agonists.

A

Clonidine, methoxamine, adrenaline, noradrenaline

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5
Q

Give examples of alpha-1 adrenoceptor antagonists.

A

Prazosin, phentolamine, phenoxybenzamine

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6
Q

Give examples of alpha-2 adrenoceptor antagonists.

A

Yohimibine, phentolamine, phenoxybenzamine

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7
Q

Give examples of clinical uses of adrenoceptor agonists.

A

Reduction of intra-ocular pressure in chronic simple glaucoma
Prolong effects of local anaesthetics
Reduce systemic toxicity
Offset hypotension in spinal/epidural anaesthesia

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8
Q

Give examples of clinical uses of adrenoceptor antagonists.

A

Treatment of adrenal medulla tumours

Dilation of arterioles and veins

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9
Q

What is tamsulosin and what is its clinical use?

A

An alpha-1 antagonist used in benign prostatic hyperplasia, relaxing the prostate to prevent the urethra from being blocked

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10
Q

Give examples of beta-1 adrenoceptor agonists.

A

Dobutamine, isoprenaline, adrenaline, noradrenaline

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11
Q

Give examples of beta-2 adrenoceptor agonists.

A

Salbutamol, isoprenaline, adrenaline

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12
Q

Give examples of beta-1 adrenoceptor antagonists.

A

Atenolol, propranolol

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13
Q

Give examples of beta-2 adrenoceptor antagonists.

A

Butoxamine, propranolol

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14
Q

Why is propranolol contraindicated in asthma?

A

Because it is a non-selective beta-receptor antagonist so may cause bronchospasm which could be fatal in an asthma sufferer.

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15
Q

What are the side effects of beta-2 agonists when taken orally?

A

Tremors
Tachycardia
Hypokalaemia

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16
Q

What is the most common indication for a beta-2 agonist?

A

Asthma relief

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17
Q

Give two examples of indications for salbutamol.

A

Asthma

Suppression of premature labour

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18
Q

What are the common indications for non selective or beta-1 selective adrenceptor antagonists?

A

Hypertension
Reduction of aqueous humour in chronic simple glaucoma (timolol)
Controlling symptoms of thyrotoxicosis
Migraine prophylaxis

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19
Q

How do beta-receptor antagonists treat hypertension?

A

Reduce cardiac output
Reduce release of renin due to reduced kidney perfusion
Reduce sympathetic tone

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20
Q

How are beta antagonists useful in angina prophylaxis?

A

Reduce cardiac rate and force, thus prolonging diastole and increasing oxygen supply to coronary arteries

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21
Q

Give examples of muscarinic AChR agonists.

A

Pilocarpine, muscarine

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22
Q

Give examples of muscarinic AChR antagonists.

A

Hyoscine, atropine

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23
Q

Give examples of nicotinic AChR agonists.

A

Nicotine, suxamethonium

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24
Q

Give examples of nicotinic AChR antagonists.

A

Atracurium, tubocurarine

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25
Q

Clinical uses for drugs acting at muscarinic AChR.

A

Antiemetics, anti asthma, eye exams (pupil dilation), glaucoma

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26
Q

Clinical uses for drugs acting at nicotinic AChR.

A

Paralysing agents, nicotine addiction, Alzheimer’s, Parkinson’s

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27
Q

What effects do non-depolarising nAChR antagonists have? Give examples.

A

Cause flaccid paralysis, reversed by AChE inhibitors however, effects are limited when ACh concentrations increase.
Atracurium
Pancuronium used in euthanasia

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28
Q

What effects do depolarising nAChR antagonists have? Give examples.

A

Sustained depolarisation, leading to decreased electrical sensitivity, fasciculation and flaccid paralysis. Not reversible with AChE inhibitors.
Suxamethonium
Decamethonium

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29
Q

What is Champix?

A

Varenicline

Partial agonist at CNS nAChRs used in nicotine addiction. Although expensive, long term cheaper than NRT.

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30
Q

What are muscarinic AChR agonists used for in practice? Give examples.

A

Pilocarpine used in glaucoma

Bathanechol used in bladder disorders

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31
Q

What are muscarinic AChR antagonists used for in practice? Give examples.

A

Clozapine- antipsychotic acting via dopamine receptors
Atropine used to prevent bronchial secretions during surgery
Tiotropium is a 2nd line asthma treatment
Hyoscine is used for motion sickness
Solifenacin acts on M3 receptors for bladder hyperactivity

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32
Q

How does botox work?

A

Blocks the release of ACh via breaking down of SNARE proteins

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33
Q

How do organic nitrates work to relieve angina?

A

Activation of soluble guanylyl cyclase to form cGMP, an allosteric regulator of proteins. Protein kinase G phosphorylates specific target proteins resulting in cytoplasmic calcium concentrations reducing, thus muscle relaxation and reduction in cardiac workload.

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34
Q

How do organic nitrates work to relieve angina?

A

Activation of soluble guanylyl cyclase to form cGMP, an allosteric regulator of proteins. Protein kinase G phosphorylates specific target proteins resulting in cytoplasmic calcium concentrations reducing, thus muscle relaxation.

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35
Q

What effect does the dilation induced by nitrates have on the cardiac system?

A

Reduction in central venous pressure, venous return and preload.

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36
Q

Describe the action of GTN tablets.

A

As a sublingual tablet, onset is rapid with duration of action lasting 20-30 minutes. Due to this, tolerance is unlikely.

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37
Q

Describe the action of isosorbide mononitrate tablets.

A

Orally active with a 4-5 hour half life. In the XL form, tolerance is possible so a nitrate free period is recommended.

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38
Q

What is the indication for Rociguat?

A

Chronic thromboembolic pulmonary hypertension, fibrous clots in the lungs leading to high blood pressure and right side heart failure.

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39
Q

Give examples of PDE 3 inhibitors and their action.

A

Enoximone- increase cAMP, increasing force/rate of contraction. For short term IV use in acute heart failure.
Cilostazol- relaxes smooth muscle and inhibits platelet aggregation.

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40
Q

Give examples of PDE 4 inhibitors and their action.

A

Roflumilast is used in severe COPD

Apremilast is used in active psoriatic arthritis that is unresponsive to anti rheumatics.

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41
Q

What is sildenafil?

A

A PDE 5 inhibitor marketed for erectile dysfunction and also as Revatio for pulmonary arterial hypertension.

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42
Q

What is tadalafil?

A

A PDE 5 inhibitor used in benign prostatic hyperplasia.

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43
Q

What is a common side effect of tadalafil?

A

Visual disturbances.

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44
Q

Describe the mechanism of action of ACE inhibitors.

A

Prevent the conversion of angiotensin I to angiotensin II, thus halting the renin-angiotensin system and leading to vasodilation.

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45
Q

What is the most common side effect of ACE inhibitors and why does this occur?

A

Dry cough. Due to the accumulation of bradykinin in the airways.

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46
Q

What effect does the dilation induced by ACE inhibitors have on the cardiac system?

A

Reduction in cardiac workload without affecting contractility, thus increasing cardiac output.

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47
Q

Why do the kidneys maintain perfusion upon administration of ACE inhibitors?

A

ACE inhibitors are more effective on angiotensin sensitive vascular beds, unlike the kidneys.

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48
Q

What side effects occur with ACE inhibitors?

A

Dry cough
Rash
Angioedema

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49
Q

Give two examples of contraindications of ACE inhibitors and why.

A

Pregnancy- risk of congenital abnormalities of foetus in 2nd/3rd trimester.
Renal artery stenosis- risk of progressive renal failure.

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50
Q

Describe the mechanism of action of angiotensin I receptor blockers.

A

Prevent the conversion of angiotensin I to angiotensin II via competitive inhibition of angiotensin binding. Thus reducing vasoconstriction and salt/water retention.

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51
Q

What long term benefits are associated with angiotensin I receptor blockers?

A

Improved endothelial function

Destiffening and remodelling of large arteries

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52
Q

Name the three types of calcium channel blockers.

A

Dihydropyridines
Benzothiazepines
Phenylalkylamines

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53
Q

Describe the mechanism of action of calcium channel blockers.

A

Reduce the opening of L-type calcium channels, thus preventing influx of calcium to cause vasoconstriction.

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54
Q

What effect does the dilation induced by calcium channel blockers have on the cardiac system?

A

Reducing AV node conduction, myocardial contractility, heart rate and arterial tone due to vasodilation.

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55
Q

What are the effects of chronic administration of CCBs on the cardiac system?

A

Reduced mean arterial pressure. Increase in vascular resistance and coronary blood flow

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56
Q

What are the effects of acute administration of CCBs on the cardiac system?

A

Increased cardiac output

Increased heart rate with dihydropyridines

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57
Q

What makes dihydropyridine CCBs vascular selective?

A

Favour the inactive state of L-type calcium channels, resting potential of vascular smooth muscle cells compared to cardiac myocytes is depolarised.

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58
Q

What causes cardiac selectivity of benzothiazepine

phenylalkylamine CCBs?

A

Use dependence- enhance blockade of L-type calcium channels with repeated depolarisation.

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59
Q

Give examples of side effects caused by CCBs.

A 
Headache
Constipation
Oedema
Hypotension
AV node block
Cardiodepression
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60
Q

Why are beta-blockers less commonly used in hypertension?

A

Less effective at stroke prevention and more likely to cause diabetes.

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61
Q

In what cases are beta-blockers given in hypertension?

A

Young people unable to tolerate ACEi, women of child bearing potential and those with higher sympathetic drive.

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62
Q

Give examples of side effects caused by beta-blockers.

A

Bronchoconstriction
Precipitation of cardiac failure
Raynaud’s
Hypoglycaemia

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63
Q

Where are alpha-1 receptor blockers used in hypertension?

A

To cause vasodilation where other therapies are ineffective.

64
Q

Give examples of side effects caused by alpha-1 receptor blockers.

A

Postural hypotension
Urinary incontinence
Retrograde ejaculation

65
Q

What positive effects can alpha-1 receptor blockers show within the body?

A

Reduced ratio of LDL to HDL cholesterol.

Improve symptoms of benign prostatic hypertrophy due to relaxation of bladder and prostate.

66
Q

What effect does the dilation induced by beta blockers have on the cardiac system?

A

Reduce sympathetic output to heart nodes and cardiac tissue, prevent acceleration of heart rate and contractility. Reducing cardiac output and blood pressure.

67
Q

Describe the effects of beta blockers, particularly the RAAS, and how it effects the cardiac system.

A

Blocking of beta-1 receptors in the kidneys reduce renin production thus reducing sodium and water retention in the blood, lowering blood volume. Reduces angiotensin II formation, thus aldosterone secretion, reducing peripheral resistance. Acts directly on the vasomotor centre reducing sympathetically mediated vasoconstriction.

68
Q

Describe the mechanism of action of thiazide diuretics.

A

Block the Na/Cl cotransporter in the distal convoluted tube of the kidneys, initially lowering blood volume and leading to vasodilation.

69
Q

Give examples of side effects of thiazide diuretics.

A

Reduced potassium ion levels
Reduced insulin release
Increased plasma lipids
Erectile dysfunction

70
Q

Describe the mechanism of action of loop diuretics.

A

Block the Na/K/Cl cotransporter in the ascending loop of Henle.

71
Q

Give examples of side effects of loop diuretics.

A

Hearing effects

Cause gout or hypokalaemia

72
Q

Give examples of the main indications of loop diuretics.

A

Used for treatment of oedema and resistant hypertension as well as for use in really impaired patients.

73
Q

Describe the mechanism of action of potassium sparing diuretics.

A

Block K/Na ATPase in the distal convoluted tube and collecting ducts. Have the same effects as thiazide diuretics but are able to preserve potassium levels.

74
Q

Describe the action of hydralazine.

A

Opens potassium ATP channels leading to vasodilation of mainly arteries. Given IV in hypertensive emergencies

75
Q

Give examples of complications of hydralazine use.

A

Reflex tachycardia
Interference with inositol triphosphate thus calcium release.
Can result in systemic Lupus erythematosus

76
Q

Give examples of side effects of hydralazine use.

A

Palpitations

GI disturbances

77
Q

Describe the effects of Minoxidil.

A

Vasodilator causing increased cardiac output and heart rate as well as fluid retention.

78
Q

Describe the problems with using minoxidil.

A

Extremely potent and long lasting.

Can cause peripheral oedema, hypertrichosis and GI disturbances.

79
Q

What is hypertrichosis?

A

Abnormal growth of hair, also known as Werewolf syndrome.

80
Q

Describe the action of Methyldopa.

A

Centrally acting antihypertensive. Blocks DOPA decarboxylase, reducing dopamine precursor for noradrenaline.

81
Q

Give examples of side effects of Methyldopa.

A

Dry mouth

Low heart rate

82
Q

Describe the action of clonidine.

A

Alpha-2 receptor agonist, reducing sympathetic outflow from the brain, reducing cardiac output and total peripheral resistance.

83
Q

Give examples of side effects of clonidine.

A

Fatigue
Sedaion
Sleep disturbance

84
Q

Describe the action of aliskiren.

A

Direct renin inhibitor, leading to reduced levels of angiotensin, causing vasodilation.

85
Q

Give examples of side effects of aliskiren.

A

Arthraldia
Dizziness
Hyperkalaemia
Diarrhoea

86
Q

Describe the action of heparins.

A

Increase rate of formation of antithrombin III complexes. To have anticoagulant effects, they must bind both antithrombin III and thrombin.

87
Q

What can be administered to counteract severe haemorrhage in heparin administration?

88
Q

What is Type II Heparin-induced thrombocytopenia?

A

Heparin induces formation of antibodies that activate platelets. May cause life threatening thromboembolism.

89
Q

How can type II HIT be treated?

A

Intravenous argatroban

90
Q

Which heparins are preferred for use?

A

Low MW heparin, tinzaparin, dalteparin.

Longer duration and better bioavailability.

91
Q

What are hirudins?

A

Parenteral anticoagulants that work via the inhibition of thrombin.

92
Q

Describe the action of warfarin.

A

Competitively inhibits vitamin K reductase, preventing carboxylation of factors II, VII, IX and X.

93
Q

What are the standard treatment times for warfarin?

A

3-6 months after a 1st clot but lifelong after any clots that follow.

94
Q

When are thrombin inhibitors given? Give examples.

A

After joint replacements.

Dabigatran blocks thrombin, rivaroxiban and apixaban both block factor Xa.

95
Q

Describe the action of aspirin as an anticoagulant.

A

Irreversibly blocks COX so platelets cannot resynthesise, inhibits thromboxane A2 production until new platelets are produced.

96
Q

Describe the action of epoprostenol.

A

Prostacyclin agonist given during haemodialysis to prevent platelet aggregation

97
Q

Describe the action of diprymadole.

A

Blocks phosphodiesterase, preventing the breakdown of cAMP thus mimicking the action of prostacyclin in preventing platelet aggregation.

98
Q

Describe the action of P2Y antagonists and give an example.

A

Prevent the release of ADP by active platelets, thus preventing aggregation promotion. Clopidogrel is an irreversible example.

99
Q

Describe the action of GPIIb/IIIa antagonists and give examples.

A

Block fibrinogen binding but only used in high risk patients in hospital. Abciximab, tirofiban, eptifibatide.

100
Q

Describe the action of fibrinolytics and give examples.

A

Mimic tPA, responsible for conversion of plasminogen to plasmin, to encourage the breakdown of clots, most effective within one hour of MI. Alteplase, streptokinase, tranexamic acid.

101
Q

What is the mechanism of action of statins?

A

Competitively inhibit HMG-CoA reductase, the rate limiting enzyme in cholesterol biosynthesis.
Secondary effect- increased levels of LDL receptors.

102
Q

What are the common side effects of statins?

A

Myositis and rhabdomyolysis

103
Q

What is the mechanism of action of Ezetimibe?

A

Blocks the NPC 1L1 cholesterol transporter, reducing dietary absorption.

104
Q

What is the most common side effect of ezetimibe?

A

GI disturbances

105
Q

What are resins and how do they work?

A

Bile acid sequestrants, prevent the reabsorption of bile acids so the liver must use cholesterol to replace them. Secondarily reduce dietary absorption and increase LDL receptor number.

106
Q

How do PCSK9 inhibitors work?

A

Increase the expression of LDL receptors and the LDL clearance from blood plasma.

107
Q

How do nicotinic acid derivatives manage cholesterol levels?

A

Reduce the release of vLDL, circulating TG and LDL levels and increase HDL levels via activation of GPCR.

108
Q

What effects can high doses of nicotinic acid derivatives have on the body?

A

Reduced glucose tolerance

Promote gout

109
Q

When are fibrates used in high cholesterol? How do they act?

A

Only used first line therapy with very high TG levels, act as PPAR alpha agonists. Increase lipase expression, promote LDL uptake and increase HDL.

110
Q

What are class I Vaughan Williams System drugs?

A

Sodium channel blockers, preventing initiation of AP.

111
Q

When are sodium channel blockers avoided?

A

Post heart attack as risk of sudden death increases.

112
Q

Give an example of a Vaughan Williams class 1b drug and its use.

A

Lidocaine, used as a local anaesthetic.

113
Q

Why is use dependence useful in VW class I drugs?

A

Preferentially block open and inactivated channels which makes them very active in heart tissue.

114
Q

Give an example of a VW class Ic drug.

A

Flecainide

115
Q

What is the main clinical use of VW class I drugs?

A

Ventricular dysrhythmia

116
Q

What is the main severe side effect of VW class I drugs?

A

CNS effects such as convulsions

117
Q

What are VW class II drugs?

A

Beta-blockers

118
Q

What kind of dysrhythmias are beta-blockers used for?

A

Supraventricular and ventricular dysrhythmias.

119
Q

What is the main clinical use of VW class Ic drugs?

A

Prevention of paroxysmal atrial fibrillation.

120
Q

How do beta-receptor antagonists treat dysrhythmia?

A

Reduce phase 4 depolarisation of nodes
Slow sinus rhythm
Slows the rate of discharge of the SA node
Slow conduction through AV node

121
Q

What antidysrhythmic use do beta-blockers have? (Induced by…)

A

Excessive catecholamine release
Increased tissue sensitivity to catecholamine
Following myocardial infarction

122
Q

What are the common side effects of beta-blockers?

A

Bronchoconstriction
Precipitation of heart failure
Hypoglycaemia
Cold extremities

123
Q

Give a specific side effect of propranolol.

A

Vivid dreams

124
Q

What are VW class III drugs?

A

Potassium channel blockers, also partially block sodium and calcium channels.

125
Q

How do potassium channel blockers treat dysrhythmia?

A

Prolongs AP and refractory period, slowing heart rate.

126
Q

Give an example of a VW class III drug.

A

Amiodarone, thyroid hormone analogue

127
Q

What are the side effects of amiodarone?

A 
Microcrystals in cornea
Photoxicity
Hypothyroidism
Hepatotoxicity
Bradycardia
Fibrosis/alveolitis/pneumonitis
128
Q

In which dysrhythmias should CCBs be avoided?

A

Ventricular and WPW

129
Q

What calcium channel types are found in the heart?

A

Types L and T

130
Q

Give examples of drug ligands of L-type calcium channels?

A

Verapamil

Nifedipine

131
Q

Give examples of drug ligands of T-type calcium channels?

A

Amiloride

Octanol

132
Q

What is the main clinical use of nifedipine?

A

Hypertension due to its selectivity for vasculature

133
Q

What did N-type calcium channel blockers derive from?

A

Cone snail toxins

134
Q

Name the three types of conotoxin.

A

Conus geographus- irreversible, GVIA
Conus magus- reversible MVIIA
Conus catus- reversible, CVID

135
Q

What is ziconotide and why is it advantageous to use?

A

Conotoxin MVIIA used in neuropathic pain.
No significant respiratory depression or loss of motor co-ordination.
No euphoria/stupour associated with opioid analgesics.
No need to increase drug dosage over time (tolerance).
No withdrawal symptoms on termination of drug.

136
Q

Describe the structure of digoxin.

A

Lactone
Steroid nucleus for lipid solubility
Aglycone
Sugar residues

137
Q

What are the clinical uses for digoxin?

A

AF

Sinus rhythm but still symptomatic despite treatment with ACEi and diuretic.

138
Q

Describe the action of digoxin.

A

Inhibits Na/K ATPase, increasing sodium concentration, inhibiting calcium efflux, increasing slow release calcium. Thus increasing contraction force without raising oxygen demands.

139
Q

What effects does digoxin have on the cardiac system?

A

Increase vagus nerve activity
Slows SA node firing
Improve ventricular filling

140
Q

What effects do toxic doses of digoxin have?

A

Increased sympathetic tone

Increased after depolarisation and ectopic beats

141
Q

Describe the side effects of digoxin.

A

Nausea
Vomiting
Hypokalaemia

142
Q

What is the mechanism of action of adenosine?

A

Activates A1 purinoceptors on cardiac myocytes causing the opening of K ACh channels leading to hyperpolarisation. Inhibits voltage sensitive calcium channels, reducing the slope of pacemaker potential.

143
Q

What effects does adenosine have on the cardiac system?

A

Reduced discharge rate of SA node, conduction and increased refectory period in AV node.

144
Q

Give examples of side effects of adenosine.

A

Bradycardia
Chest pain
Facial flushing

145
Q

Describe the clinical uses of adenosine.

A

Cannot be used chronically due to short plasma half life.
AV node re-entrant tachycardia
Ventricular tachycardia associated with WPW
supraventricular tachyarrhythmias that may occur under general anaesthesia

146
Q

Describe the pharmacological secondary prevention for STEMI.

A 
Long term aspirin 75mg
12 months clopidogrel or ticagrelor
Beta blocker
Ace inhibitor
Statin
Nitrates for symptoms where necessary
(PPI in over 60s to reduce GI bleeding risk)
147
Q

What is the first line treatment in acutely presenting atrial fibrillation?

A

Flecainide
Amiodarone where there is evidence of ischaemia
Anticoagulant where there is reoccurrence risk

148
Q

What is the first line treatment in hypertension?

A

If under 55- ACEi or angiotensin II blocker

If over 55 or afro-caribbean- CCB or consider thiazide in high risk of HF

149
Q

What is the second line treatment in hypertension?

A

ACEi or angiotensin II blocker
AND
CCB or thiazide diuretic

150
Q

What is the third line treatment in hypertension?

A 
ACEi or angiotensin II blocker
AND
CCB
AND
Thiazide diuretic
151
Q

What is the fourth line treatment in hypertension?

A 
ACEi or angiotensin II blocker
AND
CCB
AND
Thiazide diuretic
AND
Further diuretic (low dose spironolactone or increase dose of thiazide)
152
Q

What is the first line treatment in stable angina?

A

Beta blocker or CCB

153
Q

What is the second line treatment in stable angina?

A

Beta blocker
AND
CCB

154
Q

What is the third line treatment in stable angina?

A 
Beta blocker
AND
CCB
AND
One of- long acting nitrate, ivabradine, nicorandil,
ranolazine
155
Q

What is the first line treatment in heart failure?

A

ACEi
AND
Beta blocker

156
Q

What is the second line treatment in heart failure?

A

Aldosterone antagonist (mild-moderate)
OR
Angiotensin II receptor blocker (mild-moderate)
OR
Hydralazine with nitrate (Afro-Caribbean or moderate-severe)

157
Q

Describe additional treatment options (as well as guidelines) for heart failure.

A

Digoxin- worsening/severe HF
Diuretics for symptom relief
CCB (amlodipine) considered in comorbid angina/hypertension
Amiodarone
Anticoagulants- sinus rhythm, previous thromboembolism
Intropic agents- short term IV use

Pharm Y2S1 (8 decks)

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