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Pharmacology > Cardiovascular (year 2) > Flashcards

Cardiovascular (year 2) Flashcards

1
Q

where is heart rate/rhythm controlled?

A

CV centre in the medulla oblongata

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2
Q

what features may we want to affect in CV pharmacology?

A

heart rate/rhythm, contractility, ventricle relaxation, preload, after load, perfusion, arterial pressure

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3
Q

what are positive/negative inotropes?

A

increase/decrease contractility

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4
Q

what are lusiotropes?

A

affect relaxation

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5
Q

what are positive/negative chronotropes?

A

increase/decrease heart rate

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6
Q

why is tachyarrhythmias a problem?

A

reduced diastolic filling time so decreases CO

more work of cardiac muscle leading to myocardial hypertrophy

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7
Q

what are the 4 classes of antidysrhythmics?

A

I - sodium channel blockers
II - beta blockers
III - potassium channel blockers
IV - calcium channel blockers

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8
Q

how do class I antidysrhythmics work?

A

bind to and block fast sodium channels meaning slower depolarisation

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9
Q

all class I antidysrhythmics exhibit use dependent sodium channel blockade, what does this mean?

A

they affect open/refractory channels over resting ones so work better on more active channels

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10
Q

what ion do class I antidysrhythmics depend on being at normal concentration to work effectively?

A

potassium - hypokalaemia reduces their function

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11
Q

why do class I antidysrhythmics only reduce heart rate in tachyarrhythmias?

A

they don’t directly affect nodal tissue

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12
Q

describe the strength of the sodium channel blockade of each group of class I antidysrhythmics

A

Ia - moderate
Ib - weak
Ic - strong

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13
Q

how do each of the groups of class I antidysrhythmics effect the effective refractory period?

A

Ia - increases it
Ib - decreases it
Ic - no change

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14
Q

when do Ib antidysrhythmics bind to their target?

A

during phase 0, this prevents premature beats as they dissociate just in time for another action potential

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15
Q

give an example of a class Ia antidysrhythmics

A

quinidine

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16
Q

how is quinidine administered?

A

orally or parenterally

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17
Q

quinidine has a channel blocking effect but also has another effect, what is this?

A

vagolytic

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18
Q

when is quinidine used?

A

atrial fibrillation in horses and farm animals

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19
Q

describe the adverse effects of quinidine

A

negative inotrope, vasodilation, rhythmic disturbance if blockade persists, GI signs

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20
Q

name a Ib antidysrhythmics

A

lidocaine

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21
Q

how is lidocaine administered?

A

parenteral (slow IV) due to almost complete first pass hepatic metabolism

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22
Q

what cells does lidocaine mainly effect?

A

diseased cells

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23
Q

what are the adverse effects of lidocaine?

A

hypotension at toxic levels, seizures, disorientation, nausea, excitement

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24
Q

what animals are particularly sensitive to lidocaine?

A

horses and cats

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25
Q

give an example of a Ic antidysrhythmics

A

flecainide

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26
Q

what beta channels do class II antidysrhythmics block?

A

beta1 - relatively selective but this is lost at higher doses

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27
Q

what effect will blocking beta2 channels have?

A

vasoconstriction

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28
Q

what effects do class II antidysrhythmics have?

A

slow calcium influx so slow pacemaker potential
slow conduction through AV node due to increased refractory period
negative inotrope and lusiotrope

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29
Q

what would class II antidysrhythmics be used for?

A

supraventricular or ventricular tachycardia

hypertension

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30
Q

give an example of a class II antidysrhythmics

A

atenolol

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31
Q

how do class III antidysrhythmics work?

A

prolong cardiac action potential by blocking potassium channels to increase refractory period and slow repolarisation

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32
Q

give an example of a class III antidysrhythmics

A

sotalol

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33
Q

what are the adverse effects of sotalol?

A

hypotension and bradycardia due to AV block, GI signs

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34
Q

what channels do class IV antidysrhythmics block?

A

calcium channels on myocytes, nodal tissue and smooth muscle

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35
Q

how do class IV antidysrhythmics slow heart rate?

A

shorten the plateau phase and slow conduction at SAN and AVN causing a partial AV block

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36
Q

what other effects to class IV antidysrhythmics have?

A

negative inotrope, positive lusiotrope and vasodilator

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37
Q

give an example of a class IV antidysrhythmics

A

diltiazem

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38
Q

how is diltiazem administered?

A

orally or parenterally (extensive first pass hepatic metabolism)

39
Q

what are the adverse effects of diltiazem at toxic levels?

A

AV block, myocardial depression, hypotension

40
Q

name another antidysrhythmics that doesn’t fall into any of the IV classes

41
Q

what is digoxin used for?

A

negative chronotrope and vagomimetic

42
Q

how does digoxin reduce heart rate?

A

slow conduction through AV node by increasing refractory period

43
Q

how is digoxin administered?

A

orally or IV

44
Q

what are the side effects of digoxin?

A

myocardial toxicity and GI toxicity

45
Q

name the classes of drug used to treat bradyarrhythmias

A

sympathomimetics, anticholinergics, methylxanthines, PDE III inhibitors

46
Q

what are two classes of sympathomimetics? give an example of each

A

beta1 agonist - dobutamine

beta2 agonist - terbutaline

47
Q

how does dobutamine work?

A

increases firing rate at SAN, they are positive inotropes

48
Q

how does terbutaline work?

A

positive chrono trope nd dromotrope

49
Q

what is a dromotrope?

A

conduction

50
Q

name a anticholinergic and what it does

A

atropine is a muscarinic antagonist

51
Q

what is atropine used for>

A

anaesthesia

52
Q

what effects does atropine have on the heart?

A

postive chronotrope and dromotrope

53
Q

what is an example of a methylxanthine?

A

theophylline

54
Q

what mechanism of action does theophylline have?

A

non-selective PDE inhibitor and adenosine antagonist

55
Q

give an example of a PDE III inhibitor

A

pimobendane

56
Q

what drug groups are used as positive inotropes?

A

PDE III inhibitors, sympathomimetics, cardiac glycosides, anticholinergics

57
Q

why are PDE III inhibitors used for cardiac pharmacology?

A

PDE III is specifically found in the heart

58
Q

what does PDE stand for and what does it do?

A

phosphodiesterase, degrades intracellular cAMP so inhibiting it will increase intracellular cAMP

59
Q

what is the effect of increased intracellular cAMP?

A

activates protein kinase A, this phosphorylates calcium channels so they are more likely to open hence increasing flow of calcium into the cardiomyocytes leading to a stronger contraction

60
Q

what other effects does PDE III inhibitors have?

A

vasodilation - myosin light chain kinase is phosphorylates

tachycardia - faster calcium flow into cells

61
Q

how is pimobendane administered?

A

oral or parenteral

62
Q

what are the side effects of pimobendane?

A

inappetence, lethargy, dyspnoea, azotaemia

63
Q

what are the desired effects of pimobendane?

A

positive inotrope, vasodilator and calcium sensitiser

64
Q

name a cardiac glycoside

65
Q

how does digoxin work?

A

inhibits sodium potassium pump to increase intracellular sodium this reduces the sodium gradient and hence the calcium extrusion from the sodium calcium exchanger

66
Q

give an example of how a sympathomimetic works on the heart

A

beta1 receptors on cardiomyocytes increase the contractility

67
Q

what are the adverse effects of sympathomimetics?

A

tachycardia and increased chances of automaticity

68
Q

give three examples of drug groups used as negative inotropes

A

sympathetic antagonists (beta blockers), cholinergics, calcium channel blockers

69
Q

how can preload be altered?

A

alter venous/atrial volume and venous diameter

70
Q

how can afterload be altered?

A

change the TPR

71
Q

how can perfusion be changed?

A

alter CO, vascular diameter and circulating volume

72
Q

what do direct vasodilators act on?

A

the smooth muscle of blood vessels

73
Q

give 6 examples of direct vasodilators

A

nitrates, dopamine, calcium channel blockers, PDE III inhibitors, hydralazine, potassium channel activators

74
Q

how do nitrates work as vasodilators?

A

cause dilation via the action of nitrous oxide. It enhances the cGMP activity that activates potassium channels to inhibit calcium entry into the cell

75
Q

give two examples of nitrates used in practise and how they’re administered and their effects

A

nitroprusside - parenterally and causes arterial and venous dilation
nitroglycerincerine - percutaneously and ventilator

76
Q

give an example of a calcium channel blocker used for vasodilation

A

amlodipine

77
Q

what are the adverse effects of amlodipine?

A

hypotension, inappetence, azotaemia, reflex tachycardia

78
Q

what dilation does hydralazine cause and where are its main effects?

A

arteriodilators and coronary, cerebral, splanchnic, renal circulation

79
Q

name a PDE V inhibitor used in vasodilation

A

sildenafil - arteriodilator particularly effective on the pulmonary circulation

80
Q

what to extrinisic mechanisms to indirect vasodilators act through?

A

sympathetic system and RAAS

81
Q

give two examples of alpha1 adrenoreceptor antagonists

A

prazosin and phenoxybenzamine

82
Q

which part of the RAAS cause vasoconstriction?

A

angiotensin II

83
Q

what other factors of the RAAS will influence blood pressure and preload?

A

water retention and sodium

84
Q

name 5 drug groups that effect the RAAS

A

reninin inhibitors, ACE inhibitors, angiotensin II antagonists, aldosterone antagonists, ADH blockers

85
Q

what are the effects of ACE inhibitors?

A

vasodilation and reduced circulating volume

86
Q

give some examples of ACE inhibitors used in practise

A

enalapril, ramipril, benazepril, captopril, imidapril

87
Q

where are ACE inhibitors activated?

88
Q

how is benazepril administered?

89
Q

angiotensin II has multiple receptors, which type is blocked by antagonists?

90
Q

give an example of an angiotensin II antagonist

A

telmisartan

91
Q

what is telmisartan licensed for?

A

protein losing nephropathy in cats

92
Q

what are aldosterone antagonists used for?

A

reduce cardiac remodelling, reduce sodium and water retention, reduce potassium loss

93
Q

give two examples of aldosterone agonists

A

spironolactone and cardalis

Pharmacology (25 decks)

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