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FRCA Pharmacology > CVS Pharmacology > Flashcards

CVS Pharmacology Flashcards

1
Q

Esmolol:

Is useful in the treatment of essential hypertension

A

False. It is only given intravenously and has a short half life.

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2
Q

Esmolol:

Has a half life of 2 minutes

A

False. It is around 10 minutes.

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3
Q

Esmolol:

Is largely excreted unchanged in the urine

A

False. It is rapidly metabolised by red-cell esterases.

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4
Q

Esmolol:

Acts selectively on beta-1 receptors

A

False. It is non-selective.

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5
Q

Esmolol:

Possesses intrinsic sympathomimetic activity

A

False

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6
Q

The following statements about selective phosphodiesterase (PDE) inhibitors are true:
Inhibition of isoenzyme family No. I effects a positive inotropic action

A

False. Inhibition of isoenzyme family No. III results in positive inotropy.

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7
Q

The following statements about selective phosphodiesterase (PDE) inhibitors are true:
Inhibition of isoenzyme family No. III results in clinically important bronchodilatation

A

False. Bronchodilatation does occur but not to a clinically significant degree.

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8
Q

The following statements about selective phosphodiesterase (PDE) inhibitors are true:
They increase myocardial oxygen consumption

A

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

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9
Q

The following statements about selective phosphodiesterase (PDE) inhibitors are true:
Tachycardia is a common occurrence

A

True. There is a reflex tachycardia.

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10
Q

The following statements about selective phosphodiesterase (PDE) inhibitors are true:
Their use increases hblood pressure as a result of increased cardiac output and systemic vascular resistance.

A

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

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11
Q

Milrinone:

Is one of the bipridine derivative group of phosphodiesterase inhibitors.

A

True. Enoximone and piroximone are imidazolone derivatives.

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12
Q

Milrinone:

Is structurally related to amrinone

A

False

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13
Q

Milrinone:

It’s short half life makes it well suited to use as an infusion

A

False. It is used in infusion form but has a terminal half life of 2.5 hours. A loading dose is required.

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14
Q

Milrinone:

Doses should be reduced in end stage renal failure

A

True. 80% is excreted unchanged via the kidneys and dose reductions are required when the creatinine clearance falls to less than 30 ml/min.

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15
Q

Milrinone:

Is incompatible with intravenous frusemide when given through the same cannula

A

True

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16
Q

Clonidine:

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

A

True

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17
Q

Clonidine:

Is rapidly absorbed when given orally

A

True

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18
Q

Clonidine:

When given as premedication, it reduces the MAC by up to 50%

A

False. It does reduce MAC but only the highly selective drugs such as dexmedetomidine have lowered anaesthetic requirements to this degree.

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19
Q

Clonidine:

Discontinuation can result in hypertension

A

True. Rebound hypertension occurs on discontinuation of long term use.

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20
Q

Clonidine:

Has a diuretic effect in humans

A

True. It inhibits the release of ADH.

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21
Q

Ephedrine:

Is a catecholamine

A

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

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22
Q

Ephedrine:

Causes the stimulation of both alpha and beta adrenoceptors

A

True

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23
Q

Ephedrine:

Acts directly and indirectly on adrenoceptors

A

True. It’s main effects are from the release of noradrenaline but it also has some direct effect on receptors.

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24
Q

Ephedrine:

Is a uterine relaxant

A

False. All anaesthetic vapours are uterine relaxants.

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25
Q

Ephedrine:

Can exist in four isomeric forms, two of which are pharmacologically active.

A

False. 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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26
Q

The following are indications for the use of ACE inhibitors:

Pre-eclampsia

A

False. ACE Inhibitors are contraindicated in pregnancy.

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27
Q

The following are indications for the use of ACE inhibitors:

Essential hypertension

A

True

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28
Q

The following are indications for the use of ACE inhibitors:

Hypertension secondary to bilateral renal artery stenosis

A

False. ACE Inhibitors are contraindicated in bilateral renal artery stenosis or unilateral renal artery stenosis supplying a single kidney as renal failure may supervene.

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29
Q

The following are indications for the use of ACE inhibitors:

Following acute myocardial infarction

A

True

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30
Q

The following are indications for the use of ACE inhibitors:

Chronic congestive cardiac failure

A

True

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31
Q

Regarding Digoxin:

25% of the oral dose is absorbed

A

False. It is well absorbed orally.

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32
Q

Regarding Digoxin:

95% is bound to plasma proteins

A

False. There is insignificant binding to plasma proteins.

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33
Q

Regarding Digoxin:

It is largely excreted unchanged in the urine

A

True

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34
Q

Regarding Digoxin:

Hypokalaemia may cause raised serum levels of digoxin

A

True

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35
Q

Regarding Digoxin:

Toxicity may result in Mobitz type II heart block

A

True. All forms of heart block have been recorded in digitalis toxicity

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36
Q

The following drugs cause prolongation of the Q-T interval:

Sotalol

A

True. Sotalol, a beta blocker, 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 the Q-T interval.

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37
Q

The following drugs cause prolongation of the Q-T interval:

Quinidine

A

True

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38
Q

The following drugs cause prolongation of the Q-T interval:

Verapamil

A

False

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39
Q

The following drugs cause prolongation of the Q-T interval:

Flecainide

A

False. Flecainide, a class IC antiarrhythmic agent does not directly prolong the Q-T interval.

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40
Q

The following drugs cause prolongation of the Q-T interval:

Disopyramide

A

True

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41
Q

The following drugs have potassium sparing diuretic effects:

Elanapril

A

True. The angiotensin converting enzyme inhibitors have an anti-aldosterone effect They act as weak potassium sparing diuretics and concomittant use of such drugs should be undertaken with care.

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42
Q

The following drugs have potassium sparing diuretic effects:

Furosemide

A

False. Frusemide use can result in hypokalaemia.

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43
Q

The following drugs have potassium sparing diuretic effects:

Triamterene

A

True

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44
Q

The following drugs have potassium sparing diuretic effects:

Spironolactone

A

True

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45
Q

The following drugs have potassium sparing diuretic effects:

Flecainide

A

False. It has no diuretic effect.

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46
Q

Sodium nitroprusside:

Acts by stimulating the release of nitric oxide in vascular tissue

A

True

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47
Q

Sodium nitroprusside:

Acts as an arteriolar and venous dilator

A

False

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48
Q

Sodium nitroprusside:

Is associated with a baroreceptor mediated rise in heart rate

A

True. Is associated with a reflex tachycardia.

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49
Q

Sodium nitroprusside:

Rapidy decomposes in the presence of light

A

False. Its decomposition is surprisingly slow: 50% of its activity remains after 2 days exposure to light.

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50
Q

Sodium nitroprusside:

Is broken down by non-specific plasma esterases

A

False. Breakdown occurs in red blood cells with production of cyanomethaemoglobin.

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51
Q

The following are recognised complications of amiodarone:

Peripheral neuropathy

A

True

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52
Q

The following are recognised complications of amiodarone:

Prologation of the Q-T interval

A

True

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53
Q

The following are recognised complications of amiodarone:

Hyperthyoidism

A

True. Hypo or hyper-thyroidism may occur at higher doses.

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54
Q

The following are recognised complications of amiodarone:

Reversible restrictive lung defect

A

True. Pulmonary fibrosis, if treated early and the amiodarone stopped, may regress.

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55
Q

The following are recognised complications of amiodarone:

Optic atrophy

A

False. Corneal microdeposits rather than optic atrophy occur in long term use.

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56
Q

The following Beta-blockers are metabolised predominantly by the liver:
Labetolol

A

True

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57
Q

The following Beta-blockers are metabolised predominantly by the liver:
Propranolol

A

True

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58
Q

The following Beta-blockers are metabolised predominantly by the liver:
Atenolol

A

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

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59
Q

The following Beta-blockers are metabolised predominantly by the liver:
Metoprolol

60
Q

The following Beta-blockers are metabolised predominantly by the liver:
Sotalol

A

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

61
Q

Labetolol:

Acts on alpha and beta receptors with higher affinity for alpha-receptors

A

False. It has more affinity for beta receptors: beta:alpha 3:1 following oral ingestion and 7:1 after IV administration.

62
Q

Labetolol:

May cause retrograde ejaculation by its beta-blocking action

A

False. This can occur secondary to it’s alpha action.

63
Q

Labetolol:

Has significant intrinsic sympathomimetic activity (ISA)

A

True. It does have significant ISA.

64
Q

Labetolol:

Causes significant postural hypotension

65
Q

Labetolol:

Is contraindicated in pregnancy

A

False. It is one of the drugs used in pre-eclampsia.

66
Q

The following are natural precursors of adrenaline:

67
Q

The following are natural precursors of adrenaline:

68
Q

The following are natural precursors of adrenaline:

69
Q

The following are natural precursors of adrenaline:

70
Q

The following are natural precursors of adrenaline:

A

False. Dopamine is a precursor of adrenaline. Dobutamine is a synthetic compound.

71
Q

Hyoscine:

Is a less potent anti-sialagogue than atropine

A

False. It is a more potent anti-sialagogue than atropine.

72
Q

Hyoscine:

Does not cross the blood-brain barrier

A

False. It has central and peripheral effects, which include sedative, anti-emetic and anti-sialogogue actions.

73
Q

Hyoscine:

Is largely excreted unchanged in the urine

A

False. Only 1% is excreted unchanged.

74
Q

Hyoscine:

Is an effective anti-emetic which can be delivered transdermally

75
Q

Hyoscine:

May produce excitement and restlessness

A

True. Through paradoxical central stimulation.

76
Q

Isoprenaline:

Has alpha and beta adrenergic activity

A

False. It acts on beta-1 and beta-2 receptors only.

77
Q

Isoprenaline:

Increases peripheral vascular resistance

A

False. It causes a fall in peripheral vascular resistance via it’s beta-2 effets.

78
Q

Isoprenaline:

Is a naturally occuring catecholamine

A

False. Isoprenaline is a synthetic catecholamine.

79
Q

Isoprenaline:

May decrease mean arterial pressure

80
Q

Isoprenaline:

It’s effects are mediated via adenylate cyclase

81
Q

Hydralazine:

Dilates arterioles and veins equally

A

False. Hydralazine is predominantly an arteriolar dilator.

82
Q

Hydralazine:

It’s first pass metabolism is dependent on the acetylator status of the patient

83
Q

Hydralazine:

Increases cerebral blood flow

84
Q

Hydralazine:

May cause a lupus-like syndrome

A

True. After chronic usage. Peripheral neuropathies and blood dyscrasias have also been reported.

85
Q

Hydralazine:

Is contraindicated in pre-eclampsia

86
Q 
Nitric oxide (NO):
Is synthesised exclusively by vascular endothelium
A

False. Nitric oxide is also produced by macrophages and thrombocytes.

87
Q 
Nitric oxide (NO):
Is synthesised from L-asparagine
A

False. It is synthesised from L-arginine.

88
Q 
Nitric oxide (NO):
Is produced by the lung
89
Q 
Nitric oxide (NO):
Binds to haemoglobin with an affinity equal to that of carbon monoxide (CO)
A

False. 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.

90
Q 
Nitric oxide (NO):
Ultimately is metabolised to nitrate which is excreted by the kidneys
91
Q

The following drugs exhibit tachyphylaxis:

GTN

92
Q

The following drugs exhibit tachyphylaxis:

Ephidrine

93
Q

The following drugs exhibit tachyphylaxis:

Suxemethonium

A

False. Repeated doses can result in a prolonged dual block.

94
Q

The following drugs exhibit tachyphylaxis:

Trimetaphan

95
Q

The following drugs exhibit tachyphylaxis:

Hydralazine

96
Q

Verapamil:

Is a derivative of papaverine

A

True. Verapamil is a synthetic papaverine derivative.

97
Q

Verapamil:

Has poor oral absorption

A

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

98
Q

Verapamil:

Has a bioavailability following oral administration of about 75%

99
Q

Verapamil:

Is highly bound to plasma proteins

100
Q

Verapamil:

Is largely excreted by the kidney

A

True. 70% of metabolites are excreted by the kidney.

101
Q

Trimetaphan:

Blocks parasympathetic ganglia to produce hypotension

A

False. Trimetaphan induces hypotension by blocking sympathetic ganglia but it also exhibits some direct vasodilatation.

102
Q

Trimetaphan:

Is an arteriolar and venous dilator

103
Q

Trimetaphan:

Is inactivated by plasma cholinesterase

104
Q

Trimetaphan:

Has a long half life

A

False. It has a plasma half-life of only 2 minutes.

105
Q

Trimetaphan:

May potentiate the effect of suxemthonium

A

True. Side-effects include histamine release, mydriasis, and potentiation of suxemthonium, urinary retention and impotence due to the non-selective ganglion blockade.

106
Q

Phenoxybenzamine:

Is a non-selective alpha-adrenergic antagonist

A

True. Phenoxybenzamine is a non-selective alpha blocker.

107
Q

Phenoxybenzamine:

Acts predominantly on pre-synaptic alpha-1 receptors

A

False. It predominantly acts post-synaptically.

108
Q

Phenoxybenzamine:

Can be given orally or intravenously

109
Q

Phenoxybenzamine:

May result in nasal stuffiness

A

True. Doses are often limited by this, along with postural hypotension.

110
Q

Phenoxybenzamine:

Is useful in the management of craniopharyngioma

A

False. It is often used in the treatment of phaeochromocytomas

111
Q

The following are side effects of thiazide diuretics:

Hyperuricaemia

112
Q

The following are side effects of thiazide diuretics:

Hyponatraemia

113
Q

The following are side effects of thiazide diuretics:

Hypoglycaemia

A

False. They can cause hyperglycaemia.

114
Q

The following are side effects of thiazide diuretics:

Hypokalaemic, hypochloraemic acidosis

A

False. Thiazides tend to result in hypokalaemic, hypochloraemic metabolic alkalosis.

115
Q

The following are side effects of thiazide diuretics:

Hypercalcaemia

116
Q

Ephedrine is unlikely to be effective in reversing hypotension in patients chronically receiving the following medication:
Reserpine

A

True. Indirectly acting sympathomimetics like ephedrine are unlikely to increase blood pressure in patients taking drugs which alter neuronal storage, uptake, metabolism or release of neurotransmitters. Reserpine depletes neuronal granules of noradrenaline.

117
Q

Ephedrine is unlikely to be effective in reversing hypotension in patients chronically receiving the following medication:
Alpha-methyl dopa

A

True. Alpha-methyl dopa acts as a false transmitter.

118
Q

Ephedrine is unlikely to be effective in reversing hypotension in patients chronically receiving the following medication:
Phenoxybenzamine

A

True. Phenoxybenzamine and propranolol block peripheral receptors and industrial doses of directly acting sympathomometics may be required to overcome their blockade.

119
Q

Ephedrine is unlikely to be effective in reversing hypotension in patients chronically receiving the following medication:
Clonidine

A

False. Clonidine works on central adrenergic receptors and the peripheral effect of indirectly acting sympathomimetics is not decreased, in fact smaller doses may be required due to receptor up regulation.

120
Q

Ephedrine is unlikely to be effective in reversing hypotension in patients chronically receiving the following medication:
Propranolol

121
Q

The following statements are true:

ACE Inhibitors slow the onset of chronic renal disease secondary to hypertension

A

True. ACE Inhibitors do slow the onset of chronic renal disease secondary to hypertension and diabetes.

122
Q

The following statements are true:

Angiotensin II causes glomerular afferent arteriolar vasodilatation

A

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

123
Q

The following statements are true:

The fetus has high renin and angiotensin II levels

A

False. Renin levels are high, but angiotensin II levels are low due to the limited pulmonary blood flow.

124
Q

The following statements are true:

Angiotensin II stimulates the release of aldosterone from the adrenal medulla

A

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

125
Q

The following statements are true:

All ACE inhibitors have similar antihypertensive efficacy at equipotent doses.

126
Q

The following may be used to control the ventricular rate in atrial fibrillation:
Quinidine

A

False. Although it may be used in atrial arrhythmias, it has a slight vagolytic effect and may accelerate the ventricular rate in AF unless digoxin is given concomitantly.

127
Q

The following may be used to control the ventricular rate in atrial fibrillation:
Atenolol

128
Q

The following may be used to control the ventricular rate in atrial fibrillation:
Amiodarone

129
Q

The following may be used to control the ventricular rate in atrial fibrillation:
Digoxin

130
Q

The following may be used to control the ventricular rate in atrial fibrillation:
Disopyramide

A

False. Disopyramide has both class Ia and III activity and an anticholinergic effect. For similar reasons to quinidine it should not be used for AF alone.

131
Q

In the treatment of cardiogenic shock:

Enoximone increases the left ventricular end diastolic pressure

A

False. It reduces afterload i.e. left ventricular end diastolic pressure due to it’s vasodilating effects.

132
Q

In the treatment of cardiogenic shock:

Adrenaline increases the systemic vascular resistance

A

True. Adrenaline acts on both alpha and beta receptors. At low doses, beta effects predominate (tachycardia, increased cardiac output, lower SVR) but at higher doses alpha effects take over with peripheral vasoconstriction.

133
Q

In the treatment of cardiogenic shock:

Cardiac output is increased by noradrenaline

A

False. Noradrenaline is mainly an alpha-agonist and increasing systemic vascular resistance and hence reducing cardiac output.

134
Q

In the treatment of cardiogenic shock:

Isoprenaline reduceses myocardial oxygen consumption

A

False. Isoprenaline produces a tachycardia viaits beta-agonist effect, increasing myocardial consumption.

135
Q

In the treatment of cardiogenic shock:

Dobutamine reduces systemic vascular resistance

A

True. Dobutamine vasodilates by acting on beta 2-adrenergic receptors.

136
Q

The following have calcium antagonistic actions on smooth muscle:
Dantrolene

A

False. Dantrolene is a direct-acting skeletal muscle relaxant. It has no action on smooth muscle.

137
Q

The following have calcium antagonistic actions on smooth muscle:
Diltiazem

138
Q

The following have calcium antagonistic actions on smooth muscle:
Nicardipine

139
Q

The following have calcium antagonistic actions on smooth muscle:
Hydralazine

140
Q

The following have calcium antagonistic actions on smooth muscle:
Nitroglycerine

A

False. Neither hydralazine nor nitrglycerine act as calcium antagonists.

141
Q

Adenosine:

Is an effective treatment stable ventricular tachycardia

A

False. 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.

142
Q

Adenosine:

Has a half life of approximately 2 minutes

A

False. It has a very short half life (<10 seconds).

143
Q

Adenosine:

Should be given as slow intravenous bolus

A

False. Beacause of it’s very short half life, it should be given as a rapid bolus.

144
Q

Adenosine:

Can result in wheezing

A

True. Though all side effects should be short lived due to it’s short half life.

145
Q

Adenosine:

Causes coronary vasoconstriction

A

False. It is a potent coronary vasodilator and may cause coronary steal in susceptible patients.

FRCA Pharmacology (13 decks)

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