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Year 2 Cardiovascular > Drugs > Flashcards

Drugs Flashcards

1
Q

What condition is more common in practice tachy or Brady cardia

A

Tachy

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2
Q

Bradycardia is managed with drugs however because part of the process is broken these are usually ineffective- what does the patient ideally need

A

A pacemaker

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3
Q

Think about how the heart deals with bradycardia and list 4 drugs types that could be used

A

Sympamimetics
Anticholinergics
Methylxanthines
PDE3 inhibitors

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4
Q

Recap of ANS: which receptors are sympathetic/parasympathetic, where are they found and what do they do when stimulated

A

A1 and A2 on non essential vessels, symp, so vasoconstriction

B1 on cardiac myocytes, symp, so inc HR and contractility

B2 on coronary and skeletal vessels, symp, so vasodilate

M2 on cardiac myocytes, parasymp so dec HR

M3 on some vessels (but remember most vessels don’t have a parasymp supply) only skeletal, coronary, genitals…. Parasymp so dilate

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5
Q

Sympamimetics are non specific so act on both b1 and b2 receptors. Give an example of a B1 agonist and a B2 agonist used to inc HR

A

B1 agonist = dobutamine

B2 agonist = terbutaline

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6
Q

Sympamimetics are not commonly used as they have lots of side effects. What situation IS dobutamine used in??

A

Horse GA to maintain BP

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7
Q

Give an example of an anticholinergic (muscarinic antagonist)

A

Atropine

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8
Q

What does atropine do?

A

It blocks the parasymp effect as its a anticholinergic

It therefore increases heart rate and can also be used to dilate pupils for examination (remember in fight or flight pupils dilate)

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9
Q

1 of the 4 drug types used is ‘methylxanthines’ give an example of one and what does it do

A

Theophylline

It is an adenosine antagonist

It stops adenosine hyper polarising the cells therefore slowing pacemaker potential

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10
Q

What is a PDE3 inhibitor?? What does it do to cardiac muscle and smooth muscle

A

PDE3 inhibitors stops PDE3 from breaking down Camp. Camp in heart muscle, activates protein kinase A which phosphorylates ca channels, increasing calcium in the cell, causing calcium induced calcium release which inc HR and contractility

In smooth muscle, CAMP inhibits formation of myosin light chain kinase and therefore cross bridges cannot be formed and the muscle doesn’t contract therefore it causes vasodilation

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11
Q

Give an example of a PDE3 inhibitor

A

Pimobendan

Known as vetmedin

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12
Q

In what situation would you NOT use drugs that increase contractility of the heart

A

When the patient has aortic stenosis. This would increase damage of the myocardium

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13
Q

What is the ONE cardiac glycoside- and what does it do??

A

Digoxin

It’s debated that it’s a positive ionotrope. However it stops Na leaving cells so its main function is to slow the heart therefore it’s not really effective in these situations

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14
Q

What do these do…

Pos chronotrope

Pos ionotrope

Pos lusiotrope

Pos domotrope

A

Inc HR

Inc contract

Inc relaxation

Inc speed of conduction

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15
Q

What do antiarrythymias always do to yhe heart rate

A

Slow it

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16
Q

What does it mean if a drug is highly protein bound

A

It means that if you give other protein bound drugs, the dose of the drug given will be increased in plasma due to competition for protein bounding which lay lead to toxicity

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17
Q

How does the heart control and alter HR

What is conduction reliant on

A

Uses ANS (CV centre in medulla)

Normal activity of and normal intracellular amounts of Ca/Na/K, and also working intercalated discs

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18
Q

What might causes an increased HR

A

Ectopic pacemakers (cells that have gained automaticity due to damage)

Damage to conducting tissues

Depression of the CV centre e.g. During anaesthetic

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19
Q

Why is a tachyarrythmia bad?

A

It reduces diastolic filling time therefore decreases EDVV, therefore dec CO and SV

In severe cases, because the cardiac output cant keep up the animal can just collapse and even suddenly die

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20
Q

What other thing other than dec CO can a tachyarrythmia result in

A

Inc work therefore myocardial hypertrophy

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21
Q

Thinking about what the heart needs to regulate HR and also maintain normal conduction how can we slow the heart?

A

Suppress the sympathetic nervous system

Activate the parasympathetic system

Block ion channels (in conduction AP)

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22
Q

How many classes of antiarrythymias are there? What does each broadly do??

A

There are 4, but a 5th can be considered for miscellaneous drugs which don’t fit into 1-4

1: block Na channels
2: beta blockers
3: k blockers
4: ca blockers

Remember never blank Katie’s cat

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23
Q

What is a side effect of ALL antiarrythymias

A

They can cause an arrhythmia

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24
Q

Give some facts about type 1 antiarrythymias

A

They block active Na fast channels

They reduce a fast heart rate but don’t affect a normal heart rate as they don’t effect nodal tissue (remember these have funny Na channels instead)

They require normal K to function- if decreased there action is dec, if inc increased etc,

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25
Q

Order these in most strongly bound to least strongly bound (dissociate fastest)

A

1c

1a

1b

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26
Q

1b intermediately dissociate what does this mean

A

They are dissociated ready for the next AP

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27
Q

Give an example of a 1a Na blocker

When is it used

A

Quinidine

Only in horses with AF, when nothing is structurally wrong with the heart, to reset the heart so SAN takes over again

Never used in small animals

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28
Q

Quinidine has a vagolytic effect. This is why we must monitor ECG carefully. What does this mean??

A

It can actually increase HR

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29
Q

Give an example of 2 1b Na blockers

A

Lidocaine

Mexiletine

30
Q

What does complete first pass metabolism mean

A

Concentration of the drug is greatly reduced before it reaches systemic circulation

31
Q

Which animals are particularly sensitive to lidocaine?

A

Horses and cats

32
Q

Beta blockers lose their selectivity at high doses what does this mean

A

They are supposed to block B1 but instead they block beta 2 and unfortunately therefore cause some vasoconstriction in skeletal and coronary arterioles

33
Q

3rd generation beta blockers also block so,e alpha receptors. What does this mean???

A

It means A1 and 2 on non essentials arterioles are blocked which would usually constrict. This means blood supply is not cut off to them. This decreases risk of kidney disease/gut necrosis

34
Q

What do beta blockers actually do

A

Slow pacemaker potential by slowing ca influx

Slow conduction so increase the refract period

Negative ionotrope and negative lusiotrope too

35
Q

In what situation would you use a beta blocker then

A

Supra ventricular and ventricular tachycardias

Hypertension

36
Q

What animals would beta blockers be no good with

A

Animals in heart failure as they reduce contractility as well as HR

37
Q

Give an example of a beta blocker

What would an adverse effect be?

A

Atenolol

Decreased contractility so reduce CO

38
Q

If class 3 block K channels what does this mean??

A

Slower hyper polarisation

Therefore increase refract period

Shown on ECG as inc QT interval

39
Q

Give an example of a class 3

A

Sotalol

Racemic mix of 2 isomers: 70% K block and 30% beta blocker

40
Q

What are possible side effects of sotalol

A

Bradycardia

Hypotension (remember beta blockers can cause vasodilation also- might not want this)

Av block

41
Q

Class 4 drugs block Ca channels, what would this cause

In which situation would all this be helpful

A

Reduced HR, reduced contractility, increased relaxation and also smooth muscle dilation

Cat with hypertrophic cardiomyopathy

42
Q

Give an example of a class 4

A

Diltiazem

Known as HyperCard (think hyper cat =cat with hypertrophic cardiomyopathy)

43
Q

What drugs fall into the class 5/misc category

What is there effect

A

Digoxin- negative chronotrope AND positive ionotrope

It’s vagomimetic (mimics vagus nerve which is parasympathetic)

It slows conduction through av node by increasing refract period

Therefore it’s good in supra ventricular tachycardia

44
Q

How can we effect preload, afterload, perfusion and systemic arterial pressure SAP

A

Preload: inc vascular diameter and alter venous volume

Afterload: alter TPR

Perfusion: alter CO, Vascular diameter and circulating volume

SAP: alter CO and TPR

45
Q

In what situation would we want to reduce preload and afterload, increase local perfusion and reduce systemic arterial pressure

A

Heart failure and hypertension

46
Q

How does the body usually alter blood flow??

A

Has both intrinsic and extrinsic mechanisms

Intrinsic: paracrine and metabolic (see other folder)

Extrinsic: RAAS, Baroreflex

47
Q

Vasodilators can be veno aterio or mixed. They can be direct or indirect- what does this mean,

A

Direct means they effect the smooth muscle of the vessel

Indirect means act on another system e.g. ANS

48
Q

Give some examples of direct vasodilators - remember these are fast acting and are things that directly effect vasculature so need to be thinking of what makes smooth muscle contract!!

A

Nitrates

Ca channel blockers

PDE3 inhibitors

Hydralazine

49
Q

What does NO do

A

Causes vasodilation in response to inc blood flow velocity

Inc No activates Cgmp which activates MLCP so cross bridges cannot form

50
Q

Nitrates work by NO action. Give some examples of nitrates

What is an expected side effect

A

Nitroglycerine

Hypotension

51
Q

In all these vasodilators what is the obvious side effect

A

Hypotension

52
Q

Give an example of a ca channel blocker

Remember these are class 4 antiarrythymias

A

Amlodipine

Only licensed for cats, no appreciable cardiac effects, hypotension side effect

53
Q

What is hydralizine

A

Arteriodilator

Mainly affects coronary, cerebral, renal and splanchnic circulation, causes a huge drop in afterload

54
Q

PDE3 inhibitors are used in congestive heart failure. What about PdE5inhibitors?? Give an example of one

A

Sildenafil (Viagra)

Effects smooth muscle more than heart 
Particularly effective in pulmonary circulation 
Inhibits breakdown of CGMP
Opens K channels 
Reduces Ca entry
55
Q

What indirect vasodilators are there?? Remember these affect other systems (ANS and RAAS)

A

Sympathetic antagonists (to stop blood vessel constriction)

ACE inhibitors

Angiotensin 2 receptor antagonists

Aldosterone antagonists

56
Q

Give some examples of alpha 1 antagonists

A

Prazosin

Phenoxybenzamine

(Not really used in practice as can act anywhere brainstem to peripheral)

57
Q

Which parts of the RAAS cause vasoconstriction

A

Angiotensin 2

ADH (vasopressin)

58
Q

What do they also do to increase blood volume pressure and therefore preload?

A

Inc Na and water retention

59
Q

What conditions therefore would benefit from RAAS blockage

A

Hypertension

Chronic renal failure

Cohesive heart failure

60
Q

What do ace inhibitors do

A

Cause vasodilation and decrease circulating volume

61
Q

When do you not use ace inhibitors

A

With renal artery stenosis

62
Q

Give some examples of ACE inhibitors

A

Benazepril

Enalapril

Ramipril

63
Q

What’s different about benazepril??

A

Other ACE inhibitors are excreted by kidney but benazepril isn’t!! This is why it’s a good choice with patients with renal function compromise! It’s excreted mostly in bile instead

64
Q

Why are angitensin 2 receptors blockers used if we have ACE inhibitors??

A

Ace is not the only enzyme capable of producing AT2.

Chymase for example is too

65
Q

Give an example of a at2 receptor blocker/antagonist??

A

Telmisartan

Known as semintra

66
Q

Aldosterone antagonists retention water and Na retention but also cause another thing which must be monitored closely- what is this??

A

They reduce K secretion and therefore K level must be monitored carefully

67
Q

Aldosterone reduces water retention what else does this mean it reduces

A

Cardiac remodelling

68
Q

Give an example of aldosterone antagonists

A

Spironalactone

69
Q

What is cardalis

A

A mix of benazepril (ACE inhibitor) and spironalactone (aldosterone inhibitor)

Therefore used for vasodilator and decreasing BP and cardiac remodelling

70
Q

What one other drug type could reduce preload

A

Diuretics

Make you lose water more

71
Q

What drugs would you use to reduce BP initially.

A

Ca channel blocker

PDE5

Hydralizine

72
Q

Why would you not use ACE inhibitors initially

A

They would have little effect

Year 2 Cardiovascular (4 decks)

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