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Year 2 NSF > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Do do positive and negative inotropes do, what are positive inotroped used to treat?

A

Positive inotropes- increase contractility
Used for dilated cardiomyopathy
Negative inotropes- decrease contractility

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2
Q

What do lusiotropes, positive and negative chronotropes do and what are they used to treat?

A

Lusiotropes- relax ventricles- used for hypertrophic and restrictive cardiomyopathy

Positive chronotropes increase HR- used for AV block
Negative chronotropes decrease HR- used for atrial fibrillation

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3
Q

What is heart rate determined and altered by?

A

CV centre in medulla oblongata

Autonomic nervous system

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4
Q

What is the conduction of the action potential of the heart dependent on?

A

Normal activity of Na, K, Ca2+ channels
Normal intracellular and extracellular concs of ions
Correct function off intercalated disks

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5
Q

Why can control of HR go wrong?

A

Ectopic pacemakers
Damage to conducting tissue
Depression of CV centre

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6
Q

Why are tachycardias a problem?

A

Reduced diastolic filling time
Lower end diastolic ventricular volume
Lower stroke volume= lower cardiac output
Increased cardiac work= hypertrophy

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7
Q

What is the name of the classes of antidysrhythmics and what are the different classes?

A

Vaughan-Williams classification

Classes- I, II, III, IV, mis (V)

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8
Q

What does each class (I ,II, III, IV) do?

A

I- sodium channel blockers
II- Beta blockers
III- Drugs which prolong AP by blocking some K channels
IV- calcium channel blockers

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9
Q

What do class I drugs bind to and what do they cause?

A

Bind to and block fast sodium channels- use dependent Na channel blockade (open over resting)
Cause reduced heart rate in tacyarrhythmias while not significantly affecting normal heart rates

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10
Q

What does the efficacy of class I sodium channel blockers depend on?

A

Normal concentration of extracellular K
Hypokalaemia reduces their function
Hyperkalaemia increases their function

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11
Q

What are the three sub-classes of Class I sodium channel blockers and how do their actions differ?

A

Ia- old, intermediate rate of dissociation
Ib- bind during phase 0, begin to dissociate for the next AP, prevents premature beats
Ic- bind and dissociate slowly, reach steady state and reduce His-purkinje system

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12
Q

Name an example of each sub-class of sodium channel blockers?

A

Ia- quinidine- increase effective refractory period
Ib- lidocaine - decrease effective refractory period
Ic- flecainide- doesn’t affect effective refractory period

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13
Q

How is quinidine (class Ia) administered and what are its adverse effects?

A

Oral or parenteral- not IV
Adverse- Various rhythm disturbances as blockage persists, negative inotropy and vasidilation, GI signs, nervousness, depression

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14
Q

How is lidocaine administered and what are its adverse effects:

A

Parenteral (slow IV) as almost complete first pass hepatic metabolism
Adverse- CNS- excitation, disorientation, seizures, nausea

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15
Q

What is the effect of class II antidyshrthmics?

A

B2 blockade- some vasoconstriction
Slow pacemaker potential by slowing calcium influx
Slow conduction through AV bundle- increase refractory period
Negative isotropy and reduced myocardial relaxation

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16
Q

What are class II antidysrythmics used for?

A

Supraventricular or ventricular tachycardias

Hypertension

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17
Q

What is an example of class II and what are its adverse effects?

A

Atenolol- beta 1 selective

Adverse effects limited to CNS

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18
Q

What are the 2 modes of actions of class III?

A

Prolong cardiac AP

Block K+ channels- slows repolarisation, increases refractor period

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19
Q

Name an example of class III antidysrhythmics and what is it made up of and what are its adverse effects?

A 
Sotalol
Racemic mixture of isomers I and D
I- non-selective beta blocker
D- inhibits K channels 
Adverse- hypotension, bradycardia, GI signs
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20
Q

What is the mode of action of class IV and therefore their effect?

A

Block ca channels of cardiomyocytes, nodal tissue, vascular and smooth muscle
Effect- shorten plateau phase, slow conduction in SAN and AVN
Negative inotropes and positive lusiotropes

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21
Q

Name an example of class IV, how is it administered?

A

Diltiazem
Oral and parenteral administration
Toxicity- myocardial depression, hypotension, AV block

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22
Q

Name an example of Class ‘V’, what is its mode of action, how is it administered, what are its adverse effects?

A

Digoxin
MOA- chronotropic effects without negative inotropy
Oral admin
Adverse- myocardial toxicity, GI toxicity

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23
Q

How are bradyarrythmias treated?

A 
Most require pacemaker if causing clinical signs
Sympathomimetics
Anticholinergics
Methylxanthines 
PDE III inhibitors
24
Q

What are examples of categories of sympathomimetics and anticholinergics and what do they do?

A

Beta 1 agonists- dobutamine- inotropic
Beta 2 agonists- terbutaline- +ve chronotropy
Muscarinic antagonists- atropine- +ve chronotropy

25
Q

Name an example of methylxanthines/PDE III inhibitors?

A

Methylxanthines- theophylline

PDE III inhibitor- Pimobendan

26
Q

What are the endogenous mechanisms of positive inotropes?

A

Endogenous increase of contractility

Sympathetic stimulation/stretch increases Ca and increases EDVV

27
Q

What drug groups are used for positive inotropy?

A 
PDE III inhibitors
Sympathomimetics
Cardiac glycosides
Anticholinergics
Glucafon
28
Q

When would positive inotropes not be used?

A

If there is is aortic/pulmonary stenosis

29
Q

What is the mode of action of PDE III?

A

Increases intracellular cAMP by inhibiting phosphodiesterase which degrades it
cAMP activates protein kinase A, which phosphorylates a site on ca channels making them more likely to open, increased ca release- stronger contraction

30
Q

What are the side effects of PDE III and why?

A

Vasodilation- cAMP activates a kinase which phosphorylates myosin light chain kinase, this prevents phosphorylation of myosin- relaxation
Tachycardia- faster Ca flow= faster depolarisation

31
Q

What is an example of a PDE III inhibitor and what are its adverse effects?

A

Pimobendan
oral or parenteral
Adverse- inappetence, lethargy, dyspnoea, azotaemia

32
Q

What cardiac glycoside is used in practice and what is its ‘supposed’ mode of action?

A

Digoxin
MOA- inhibit Na/K pump in cardiac myocyte- increased intracellular NA, reduced Ca extrusion via Na/Ca exchanger, therefore more Ca into SR for AP

33
Q

What is the mode of action of sympathomimetics, predict its side effects, and what is their other use?

A

B1 receptors on cardiac myocytes- agonist action increases contractility
Side effects- tachycardia, increased risk of automaticity
used for anaesthesia

34
Q

What are the three types of negative inotropes?

A

Sympathetic antagonists- beta blockers
Cholinergics- antagonises sympathetic action on cardiomyocytes via M2 receptor
Calcium channel blockers- reduced calcium influx

35
Q

How can drugs affect vessel diameter and blood volume?

A

Affect preload
Affect afterload
Affect perfusion
Affect arterial pressure

36
Q

How can preload, after load, perfusion, systemic arterial pressure be changed?

A

Preload- alter venous/atrial volume, venous diameter
Afterload- alter TPR
Perfusion- CO, vascular diameter, circulating volume
Systemic arterial pressure- CO, TPR

37
Q

How can venodilators act?

A

Direct- smooth muscle (faster)

Indirect- affect another system

38
Q

Name types of drugs which are direct vasodilators?

A 
Nitrates
Dopamine
Ca channel blockers
PDE III inhibitors
Hydralazine
K channel activators
39
Q

What is the mode of action of nitrates?

A

Peripheral vasodilation

cGMP activates K channels, inhibits Ca2+ entry into cell and activates PK-G which activates MLCP- causes relaxation

40
Q

What two nitrate drugs are used in practice?

A

Nitroprusside- given parenterally, causes mixed arterial and venodilation- can lead to cyanide poisoning
Nitroglycerine- venodilator- causes hypotension

41
Q

What class of antidysrythmics are Ca++ blockers and what drug is used as a vasodilator?

A

Class IV

Amlodipine- hypotension, taccycardia

42
Q

What does hydralazine cause and where, predict its adverse effects?

A

Arteriodilator- coronary, cerebral, renal, splanchnic
Reflex tacycardia
Adverse effects- hypotension

43
Q

What PDE V inhibitor is used for vasodilation, what is its mode of action?

A

Sildenafil
MOA-inhibits breakdown of cGMP- activates proteins kinase G- MLCP activates- dephosphorylates MLC- relaxation
Arteriodilator

44
Q

What two extrinisic mechanisms do indirect vasodilator act on?

A

Sympathetic

RAAS

45
Q

What are two examples of alpha 1 adrenoreceptor sympathetic antagonists?

A

Prazosin- adverse- hypotension, tachycardia

Phenoxybenzamine

46
Q

What parts of RAAS causes vasoconstriction?

A

AngII

Stimulated ADH release

47
Q

Other than Ang II and stimulated ADH release what of the RAAS affects blood pressure and preload?

A

Retained water and Na+ increases blood pressure and preload

48
Q

What conditions would benefit from RAAS blockade?

A

Congestive heart failure
Hypertension
Chronic renal failure

49
Q

What types of drugs affect RAAS?

A 
Renin inhibitors
ACE inhibitors 
AII receptor antagonists
Aldosterone antagonists 
ADH blockers
50
Q

What is the effect of ACE inhibitors and adverse effects, when are they contraindicated?

A

Cause vasodilation and reduced circulating volume- improved tissue perfusion, reduced preload and systemic arterial pressure
Adverse- uncommon- Hypotension
Contraindicates it renal artery stenosis is present

51
Q

What are the names of the ACE inhibitor drugs used in. practice, where are they activated and excreted?

A

Enalapril, Ramipril, Benzapril, Catopril, Imidapril
Activated in liver
Excreted in kidneys (except benazepril)

52
Q

What AII receptor agonists are used in practice and where is it excreted?

A

Telmisartan

Bile and urine

53
Q

What is the action of aldosterone agonists?

A

Reduce retention of sodium and water

54
Q

What aldosterone agonists are used in practice?

A

Sprionolactone

Cardalis

55
Q

What other drugs can reduce preload?

A

Diruretics- loop, thiazide, potassium sparring, osmotic

Year 2 NSF (16 decks)

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