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Pharmacology > Cardiovascular (year 2) > Flashcards

Cardiovascular (year 2) Flashcards

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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
give an example of a Ic antidysrhythmics
flecainide
26
what beta channels do class II antidysrhythmics block?
beta1 - relatively selective but this is lost at higher doses
27
what effect will blocking beta2 channels have?
vasoconstriction
28
what effects do class II antidysrhythmics have?
slow calcium influx so slow pacemaker potential slow conduction through AV node due to increased refractory period negative inotrope and lusiotrope
29
what would class II antidysrhythmics be used for?
supraventricular or ventricular tachycardia | hypertension
30
give an example of a class II antidysrhythmics
atenolol
31
how do class III antidysrhythmics work?
prolong cardiac action potential by blocking potassium channels to increase refractory period and slow repolarisation
32
give an example of a class III antidysrhythmics
sotalol
33
what are the adverse effects of sotalol?
hypotension and bradycardia due to AV block, GI signs
34
what channels do class IV antidysrhythmics block?
calcium channels on myocytes, nodal tissue and smooth muscle
35
how do class IV antidysrhythmics slow heart rate?
shorten the plateau phase and slow conduction at SAN and AVN causing a partial AV block
36
what other effects to class IV antidysrhythmics have?
negative inotrope, positive lusiotrope and vasodilator
37
give an example of a class IV antidysrhythmics
diltiazem
38
how is diltiazem administered?
orally or parenterally (extensive first pass hepatic metabolism)
39
what are the adverse effects of diltiazem at toxic levels?
AV block, myocardial depression, hypotension
40
name another antidysrhythmics that doesn't fall into any of the IV classes
digoxin
41
what is digoxin used for?
negative chronotrope and vagomimetic
42
how does digoxin reduce heart rate?
slow conduction through AV node by increasing refractory period
43
how is digoxin administered?
orally or IV
44
what are the side effects of digoxin?
myocardial toxicity and GI toxicity
45
name the classes of drug used to treat bradyarrhythmias
sympathomimetics, anticholinergics, methylxanthines, PDE III inhibitors
46
what are two classes of sympathomimetics? give an example of each
beta1 agonist - dobutamine | beta2 agonist - terbutaline
47
how does dobutamine work?
increases firing rate at SAN, they are positive inotropes
48
how does terbutaline work?
positive chrono trope nd dromotrope
49
what is a dromotrope?
conduction
50
name a anticholinergic and what it does
atropine is a muscarinic antagonist
51
what is atropine used for>
anaesthesia
52
what effects does atropine have on the heart?
postive chronotrope and dromotrope
53
what is an example of a methylxanthine?
theophylline
54
what mechanism of action does theophylline have?
non-selective PDE inhibitor and adenosine antagonist
55
give an example of a PDE III inhibitor
pimobendane
56
what drug groups are used as positive inotropes?
PDE III inhibitors, sympathomimetics, cardiac glycosides, anticholinergics
57
why are PDE III inhibitors used for cardiac pharmacology?
PDE III is specifically found in the heart
58
what does PDE stand for and what does it do?
phosphodiesterase, degrades intracellular cAMP so inhibiting it will increase intracellular cAMP
59
what is the effect of increased intracellular cAMP?
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
what other effects does PDE III inhibitors have?
vasodilation - myosin light chain kinase is phosphorylates | tachycardia - faster calcium flow into cells
61
how is pimobendane administered?
oral or parenteral
62
what are the side effects of pimobendane?
inappetence, lethargy, dyspnoea, azotaemia
63
what are the desired effects of pimobendane?
positive inotrope, vasodilator and calcium sensitiser
64
name a cardiac glycoside
digoxin
65
how does digoxin work?
inhibits sodium potassium pump to increase intracellular sodium this reduces the sodium gradient and hence the calcium extrusion from the sodium calcium exchanger
66
give an example of how a sympathomimetic works on the heart
beta1 receptors on cardiomyocytes increase the contractility
67
what are the adverse effects of sympathomimetics?
tachycardia and increased chances of automaticity
68
give three examples of drug groups used as negative inotropes
sympathetic antagonists (beta blockers), cholinergics, calcium channel blockers
69
how can preload be altered?
alter venous/atrial volume and venous diameter
70
how can afterload be altered?
change the TPR
71
how can perfusion be changed?
alter CO, vascular diameter and circulating volume
72
what do direct vasodilators act on?
the smooth muscle of blood vessels
73
give 6 examples of direct vasodilators
nitrates, dopamine, calcium channel blockers, PDE III inhibitors, hydralazine, potassium channel activators
74
how do nitrates work as vasodilators?
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
give two examples of nitrates used in practise and how they're administered and their effects
nitroprusside - parenterally and causes arterial and venous dilation nitroglycerincerine - percutaneously and ventilator
76
give an example of a calcium channel blocker used for vasodilation
amlodipine
77
what are the adverse effects of amlodipine?
hypotension, inappetence, azotaemia, reflex tachycardia
78
what dilation does hydralazine cause and where are its main effects?
arteriodilators and coronary, cerebral, splanchnic, renal circulation
79
name a PDE V inhibitor used in vasodilation
sildenafil - arteriodilator particularly effective on the pulmonary circulation
80
what to extrinisic mechanisms to indirect vasodilators act through?
sympathetic system and RAAS
81
give two examples of alpha1 adrenoreceptor antagonists
prazosin and phenoxybenzamine
82
which part of the RAAS cause vasoconstriction?
angiotensin II
83
what other factors of the RAAS will influence blood pressure and preload?
water retention and sodium
84
name 5 drug groups that effect the RAAS
reninin inhibitors, ACE inhibitors, angiotensin II antagonists, aldosterone antagonists, ADH blockers
85
what are the effects of ACE inhibitors?
vasodilation and reduced circulating volume
86
give some examples of ACE inhibitors used in practise
enalapril, ramipril, benazepril, captopril, imidapril
87
where are ACE inhibitors activated?
liver
88
how is benazepril administered?
orally
89
angiotensin II has multiple receptors, which type is blocked by antagonists?
AT1
90
give an example of an angiotensin II antagonist
telmisartan
91
what is telmisartan licensed for?
protein losing nephropathy in cats
92
what are aldosterone antagonists used for?
reduce cardiac remodelling, reduce sodium and water retention, reduce potassium loss
93
give two examples of aldosterone agonists
spironolactone and cardalis

Pharmacology (25 decks)

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