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Exam Prep MCQs > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

What is the half life of esmolol?

A

10mins

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2
Q

How is esmolol metabolised?

A

Rapidly metabolised by red-cell esterases

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3
Q

Is esmolol a selective or non-selective beta blocker?

A

Non selective

(although mainly blocks B1 receptors, only blocks B2 at high doses)

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4
Q

In selective phosphodiesterase inhibitors, inhibition of which isoenzyme family causes a positive inotropic action?

A

Isoenzyme family no III

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5
Q

In selective phosphodiesterase inhibitors, does inhibition of isoenzyme family no III cause clinically important bronchodilation?

A

No. It does cause slight bronchodilatation but not to a clinically significant degree.

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6
Q

How do selective phosphodiesterase inhibitors affect myocardial oxygen consumption?

A

There is unchanged or even slightly reduced myocardial oxygen consumption as systemic vasodilation reduces left ventricular systolic wall tension.

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7
Q

Do selective phosphodiesterase inhibitors cause a reflex tachycardia?

A

Yes

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8
Q

What effect do selective phosphodiesterase inhibitors have on BP?

A

Hypotension is often seen as a result of reduced systemic vascular resistance due to smooth muscle relaxation.

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9
Q

What is milrinone?

A

Is one of the bipridine derivative group of phosphodiesterase inhibitors.

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10
Q

What are enoximone and piroximone?

A

Enoximone and piroximone are imidazolone derivatives.

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11
Q

Is milrinone structurally related to amrinone?

A

No

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12
Q

What is the terminal half life of milrinone?

A

2.5hrs

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13
Q

Can milrinone be given as an infusion?

A

Yes but a loading dose is required. Half life is 2.5hrs.

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14
Q

How should you alter the dose of milrinone in renal failure?

A

Reduce the dose when creatinine clearance < 30ml/min.

80% is excreted unchanged via the kidneys.

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15
Q

Which drug should not be given with milrinone in the same cannula due to incompatibility?

A

Furosemide

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16
Q

What is clonidine?

A

A selective partial agonist for the alpha-2 adrenoceptor with a ratio of approximately 200:1 (alpha2 : alpha1)

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17
Q

What is the effect of clonidine when given as a premedication?

A

It’s rapidly absorbed when given orally.

It reduces the MAC, but not by as much as 50% (only highly selective drugs like dexmedetomidine can lower MAC this much)

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18
Q

What can occur on discontinuation of clonidine after long term use?

A

Rebound hypertension

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19
Q

Does clonidine cause diuresis?

A

Yes, it inhibits ADH

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20
Q

Why is ephedrine not a catecholamine?

A

It does not have a hydroxyl substitution of the benzene ring, and therefore cannot be called a catecholamine

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21
Q

Which receptor does ephedrine act on?

A

Stimulation of both alpha and beta adrenoceptors

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22
Q

What isomeric forms of ephedrine are there?

A

It can exist in four isomeric forms but the only active one is the l-form. Ephedrine is supplied as the racaemic mixture or simply in the l-form

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23
Q

What are the indications for use of ACE inhibitors?

A
  • essential hypertension
  • following acute MI
  • chronic heart failure
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24
Q

Is digoxin well-absorbed orally?

A

Yes

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25
Q

How protein bound is digoxin?

A

An insignificant amount

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26
Q

How is digoxin excreted?

A

Largely unchanged in the urine

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27
Q

Can potassium levels affect digoxin levels?

A

Hypokalaemia can cause increased digoxin levels

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28
Q

What kind of heart block can digoxin toxicity result in?

A

All types of heart block including Mobitz Type II

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29
Q

What drugs can prolong the QT interval out of the following?

(sotalol, quinidine, verapamil, flecainide, disopyramide)

A

Sotalol, quinidine, disopyramide.

Sotalol posesses class III activity, and both quinidine and disopyramide have class 1A actions with mild class III activity prolonging the cardiac action potential and hence QT interval.

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30
Q

Which drugs have a potassium sparing effect?

A

Enalapril (ACEi have an anti aldostrone effect and act as weak potassium sparing diuretics)

Triamterene

Spironolactone

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31
Q

What does sodium nitroprusside do?

A
  • stimulates release of nitric oxide in vascular tissue
  • does not dilate arterioles
  • is associated with a baroreceptor mediated rise in HR
  • decomposes slowly in response to light (50% active after 2 days light exposure)
  • broken down in RBCs with production of cyanomethaemoglobin
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32
Q

What are recognised complications of amiodarone?

A
  • peripheral neuropathy
  • prolongation of the QT interval
  • hyper/hypothyroidism
  • pulmonary fibrosis
  • corneal microdeposits
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33
Q

Which beta blockers are metabolised predominantly in the liver? Which ones are metabolised by the kidney?

A
  • labetalol
  • propranolol
  • metoprolol

Atenolol and sotalol are water soluble and therefore predominantly metabolised by the kidney.

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34
Q

What receptors does labetolol work on?

A

It has more affinity for beta receptors

Beta: alpha 3:1 (oral)

Beta: alpha 7:1 (IV)

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35
Q

How can labetolol cause retrograde ejaculation?

A

Secondary to it’s alpha action

36
Q

Does labetolol have significant intrinsic sympathomimetic activity?

A

Yes

37
Q

Can labetolol cause postural hypotension?

A

Yes

38
Q

What are the natural precursors of adrenaline?

A

Dihydroxyphenylalanine and dopamine

The synthetic pathway is as follows:

Tyrosine-DOPA-Dopamine-Noradrenaline-Adrenaline.

39
Q

What is dopexamine?

A

It’s an analogue of dopamine which acts mainly at beta2 and DA-1/DA-2 receptors.

No alpha activity.

Does not require a loading dose and is a weak positive inotrope but powerful splachnic vasodilator reducing afterload.

40
Q

Which receptors does isoprenaline work on?

A

Beta1 and 2 only.

41
Q

How does isoprenaline affect peripheral vascular resistance?

A

Causes a fall due to it’s beta2 effects

42
Q

Can isoprenaline decrease MAP?

A

Yes

43
Q

How are the effects of isoprenaline mediated?

A

Via adenylate cyclase

44
Q

What does hydralazine do?

A

An arteriolar dilator

45
Q

What is the 1st pass metabolism of hydralazine dependent on?

A

The acetylator status of the patient

46
Q

How does hydralazine affect cerebral blood flow?

A

It increases it

47
Q

What syndrome can hydralazine cause?

A

A lupus-like syndrome

48
Q

Where is nitric oxide produced?

A

Vascular endothelium

Macrophages

Thrombocytes

49
Q

What is nitric oxide synthesised from?

A

L-arginine

50
Q

How much higher affinity does Hb have for NO than CO?

A

The haemoglobin molecule has an affinity 1500 times higher to NO than to CO. Nitrosyl haemoglobin is produced, which in the presence of oxygen, is oxidised to methaemoglobin.

51
Q

What is nitric oxide metabolised to?

A

Nitrate which is excreted by the kidneys

52
Q

What drugs exhibit tachyphylaxis?

A

GTN

Ephedrine

Trimetaphan

53
Q

What is verapamil?

A

Synthetic papaverine derivative

54
Q

Is verapamil absorbed orally?

A

It is well absorbed following oral administration, but undergoes extensive first pass metabolism with a bioavailability of 10-20%

55
Q

How protein bound is verapamil?

A

~ 90%

56
Q

How is verapamil excreted?

A

70% of metabolites are excreted by the kidney

57
Q

How does trimetaphan work?

A

Induces hypotension by blocking sympathetic ganglia but also exhibits some direct vasodilatation.

It dilates both arterioles and veins.

It’s inactivated by plasma cholinesterase.

58
Q

What are the SEs of trimetaphan?

A
  • histamine release
  • mydriasis
  • potentiation of suxamethonium
  • urinary retention
  • impotence
    • due to non-selective ganglion blockade
59
Q

What is the plasma half life of trimetaphan?

A

Half life of 2 mins

60
Q

What is phenoxybenzamine?

A

Non-selective alpha blocker

61
Q

Where does phenoxybenzamine act?

A

Predominantly on post-synaptic alpha1 receptors

62
Q

Which routes can phenoxybenzamine be given?

A

Orally or IV

63
Q

What limits increasing the dose of phenoxybenzamine?

A

Nasal stuffiness and postural hypotension

64
Q

What is phenoxybenzamine used for?

A

Treatment of phaeochromocytomas

65
Q

What are the SEs of thiazide diuretics?

A
  • hyperuricaemia
  • hyponatraemia
  • hypercalcaemia
  • hyperglycaemia
  • hypokalaemia
  • hyperchloaremia
    • result in hypokalaemic, hypochloraemic metabolic alkalosis
66
Q

Ephedrine is unlikely to be effective in reversing hypotension in patient’s taking what medicines?

A

Indirectly acting sympathomimetics like ephedrine are unlikely to increase BP in patients taking drugs which alter neuronal storage, uptake, metabolism or release of neurotransmitters

  • Reserpine- depletes neuronal granules of noradrenaline
  • alpha-methyl dopa - acts as a false transmitter
  • phenoxybenzamine
  • propranolol
    • both block peripheral receptors and industrial doses of directly acting sympathomimetics may be required to overcome their blockade
67
Q

How do ACEi affect the onset of chronic renal disease secondary to hypertension?

A

They slow the onset

68
Q

What does angiotension II do to the glomerular arterioles?

A

Angiotensin II causes glomerular arteriolar vasoconstriction (in the efferent arterioles to a greater extent than the afferent)

69
Q

Does the fetus have high renin and angiotensin II levels?

A

Renin levels are high

Angiotensin II levels are low due to limited pulmonary blood flow

70
Q

Does angiotensin II stimulate the release of aldosterone?

A

Yes. Angiotensin II stimulates the release of aldosterone from the adrenal cortex.

71
Q

Do all ACE inhibitors have similar antihypertensive efficacy at equipotent doses?

A
72
Q

What drugs would you give to control ventricular rate in AF?

A
  • atenolol
  • amiodarone
  • digoxin
73
Q

What is quinidine used for?

A

Can be used in atrial arrhythmias but it has a slight vagolytic effect so can accelerate the ventricular rate in AF unless digoxin is given at the same time.

74
Q

Can disopyramide be given in AF?

A

It has class Ia and III activity and an anticholinergic effect.

It should not be given for AF by itself.

75
Q

What does enoximone do in cardiogenic shock?

A

Reduces afterload (ie LVEDP) due to vasodilating effects

76
Q

How does adrenaline affect SVR?

A
  • acts on both alpha and beta receptors
  • at low doses beta effects predominate (tachycardia, increased CO, lower SVR)
  • at higher doses alpha effects take over with peripheral vasoconstriction
77
Q

How does noradrenaline affect CO?

A

It increases SVR and hence reduces CO. It is mainly an alpha-agonist.

78
Q

What does isoprenaline do in cardiogenic shock?

A

It produces a tachycardia via it’s beta agonist effect- increasing myocardial consumption

79
Q

What effect does dobutamine have on SVR?

A

It decreases SVR by vasodilation through Beta2 adrenergic agonism.

80
Q

What is dantrolene and how does it affect calcium actions on smooth muscle?

A

It’s a direct acting skeletal muscle relaxant.

It has no action on smooth muscle.

81
Q

What drugs will have calcium antagonistic actions on smooth muscle?

A
  • diltiazem
  • nircardipine
82
Q

Which rhythms is adenosine effective in treating?

A

Adenosine is effective in SVTs, depressing the SA node activity and blocking AV node conduction. Although ineffective in VTs, it can serve to distinguish SVT with associated bundle branch block from VT in a patient with broad complex tachycardia.

83
Q

What is the half life of adenosine?

A

30 seconds

84
Q

What SE can adenosine cause?

A

Wheeze

Coronary vasodilation -therefore coronary steal in susceptible patients

85
Q
A

Exam Prep MCQs (19 decks)

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