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Cardiovascular BNF chapter > Cardiovascular drugs > Flashcards

Cardiovascular drugs Flashcards

1
Q

Clonidine is indicated for:

A

Hypertension

Prevention of recurrent migraine/ Menopausal symptoms (particularly flushing) / prevention of vascular headache

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2
Q

Clonidine is unlicensed for the treatment of:

A

Tourette syndrome and sedation

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3
Q

what is clonidine?

A

a centrally acting antihypertensive

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4
Q

what are the C/Is for methyldopa?

A

Acute porphyrias, depression, paraganglioma

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5
Q

can methyldopa be used in pregnancy or breastfeeding?

A

yes, amount in breast milk too small to be harmful

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6
Q

which drug may lower foetal HR?

A

clonidine - BNF says to avoid injection and avoid oral use unless benefit>risk

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7
Q

what are the common side effects of clonidine?

A

constipation, dry mouth, nausea, fatigue, depression, dizziness, sleep disorders, sexual dysfunction

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8
Q

methyldopa can cause tongue discolouration and burning. T or F?

A

true

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9
Q

what are the monitoring requirements for methyldopa?

A

blood count and LFTs before treatment and at intervals during the first 6-12 weeks or when unexplained fever occurs

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10
Q

moxonidine is:

A

a centrally-acting antihypertensive drug used for the treatment of mild to moderate essential HTN

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11
Q

moxonidine is C/I in:

A

Bradycardia
2nd or 3rd degree AV block
sino-atrial block
severe HF

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12
Q

Can moxonidine be used in renal impairment?

A

Avoid if eGFR less than 30ml/min/1.73m2

max. single dose is 200micrograms and max. daily dose is 400micrograms if eGFR between 30 and 60 ml/min/1.73m2

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13
Q

If moxonidine is used together with a beta-blocker, which drug should be stopped first?

A

the beta-blocker should be stopped first and moxonidine should be stopped after a few days

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14
Q

what are the common s/e of moxonidine?

A

asthenia, diarrhoea, dizziness, N+V, skin reactions, dyspepsia

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15
Q

where ca beta-adrenoceptors be found?

A

heart, lungs, pancreas, liver, peripheral vasculature

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16
Q

what does intrinsic sympathomimetic activity mean?

A

partial agonist activity; beta-blockers which stimulates as well as inhibit beta-adrenoceptors. these beta-blockers tend to cause less bradycardia and may also cause less coldness of the extremities.

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17
Q

give an example of a beta-blocker with ISA activity

A

oxprenolol
pindolol
acebutolol
celiprolol

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18
Q

name a few water-soluble beta-blockers.

A

atenolol, nadolol, sotalol

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19
Q

why do water-soluble beta-blockers cause less sleep disturbance and nightmares?

A

because they are less likely to enter the brain through the BBB (water-soluble molecules)

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20
Q

which beta-blockers have a longer duration of action and can be given once daily?

A

atenolol, bisoprolol, nadolol, celiprolol

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21
Q

which beta-blockers have an arteriolar vasodilating action and lower peripheral resistance?

A

labetalol
carvedilol
nebivolol
celiprolol

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22
Q

what are the s/e associated with beta-blockers?

A

cold extremities
fatigue
bradycardia
sleep disturbances and nightmares
hypo- or hyperglycaemia in patients with or without diabetes (affect carbohydrate metabolism)
can also interfere with metabolic or autoimmune responses to hypoglycaemia => mask tachycardia

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23
Q

which beta-blockers are relatively cardioselective and can be used in patients with well-controlled asthma, or COPD, to treat a co-existing condition (e..g HF or MI)?

A 
atenolol
bisoprolol
nebivolol
metoprolol
acebutolol (to a lesser extent)
- they have less effect on the beta2-adrenoceptors in the bronchi and on airways resistance
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24
Q

beta-blockers should be avoided in those with frequent episodes of hyperglycemia. T or F?

A

False, they should be avoided in those with frequent episodes of HYPOglycaemia

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25
Q

what is the MoA of beta-blockers in hypertension?

A

not quite understood
beta-blockers reduce CO, alter baroreceptor reflex sensitivity and block peripheral adrenoceptors
possibly a central effect is in place as well

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26
Q

beta-blockers are effective for reducing BP but other antihypertensives are more effective in reducing the incidence of stroke, MI and CV mortality. T or F?

A

True.

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27
Q

can beta-blockers be used in the treatment of phaeochromocytoma (a rare, usually benign tumour of the adrenal glands)?

A

yes, they can be used to control the pulse rate in patients. however, beta-blockers should always be given with an alpha-blocker as beta-blockade without concurrent alpha-blockade can lead to a hypertensive crisis. Therefore, phenoxybenzamine HCl should always be given with a beta-blocker.

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28
Q

sudden beta-blocker withdrawal can cause exacerbation of angina. T or F?

A

True. Therefore, a gradual reduction of the dose is preferable.

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29
Q

why should beta-blockers not be used together with rate-limiting CCB such as verapamil in the treatment of HF?

A

risk of precipitating HF and cardiac block

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30
Q

which beta-blockers can be used in MI?

A

The evidence shows that atenolol and metoprolol can be used in the acute phase of MI as they may reduce early mortality after IV and a subsequent oral administration.

metoprolol, propranolol, timolol and acebutolol have protective value when started in the early convalescent phase (recovery phase).

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31
Q

what beta-blocker is esmolol?

A

relatively cardioselective;
very short duration of action
used IV for the short-term treatment of supraventricular arrhythmias, sinus tachycardia, hypertension as well as acute MI

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32
Q

what beta-blocker is sotalol?

A

non-cardioselective with additional class III antiarrhythmic activity
used for prophylaxis in paroxysmal supraventricular arrhythmias
suppresses ventricular ectopic beats and non-sustained ventricular tachycardia

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33
Q

which non-cardioselective beta-blocker may induce torsades de pointes in susceptible patients?

A

sotalol

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34
Q

which beta-blockers reduce mortality in any grade of stable HF?

A

bisoprolol and carvedilol

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35
Q

which beta-blocker is licensed for stable MILD to MODERATE HF in pts >70years?

A

nebivolol

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36
Q

which beta-blocker can reverse clinical symptoms of thyrotoxicosis?

A

propranolol HCl

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37
Q

what is thyrotoxicosis?

A

Thyrotoxicosis describes disorders of excess thyroid hormone with or without the increased synthesis of thyroid hormone (hyperthyroidism).
Graves’ disease (GD) and toxic nodular (TN) goitre account for most cases of thyrotoxicosis associated with hyperthyroidism.
Although thyrotoxicosis typically presents with weight loss, heat intolerance, and palpitations, there are a large variety of additional features, which manifest more variably with advancing age and in people with milder disease.
Beta blocking agents are useful for symptom control, especially in older patients, and those with cardiovascular disease. Propranolol is often prescribed but longer-acting agents, eg atenolol, may result in improved compliance. Oral calcium channel blockers, eg verapamil and diltiazem, may also be used to reduce the pulse rate of patients who cannot tolerate beta-blockers.
The main therapeutic options are antithyroid drugs (thionamides), radioactive iodine and surgery.

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38
Q

which beta-blockers are used topically in glaucoma?

A

timolol
levobunolol
betaxolol

39
Q

Beta-blockers are also used in the prophylaxis of migraine. T or F?

A

True.

NB: Clonidine - a centrally acting antihypertensive is licensed for prevention of recurrent migraines

40
Q

what are the contraindications for beta-blockers?

A 
Asthma (bronchospasm)
2nd or 3rd-degree AV block
cardiogenic shock
Prinzmetal angina 
severe peripheral arterial disease 
marked bradycardia
hypotension
metabolic acidosis
uncontrolled HF
phaeochromocytoma (unless used with an alpha-blocker)
41
Q

when should beta-blockers be used with caution?

A 
diabetes
COPD
1st-degree AV block
myasthenia gravis 
portal hypotension 
psoriasis
42
Q

why should beta-blockers be avoided in people with frequent episodes of hypoglycaemia?

A

because beta-blockers can mask symptoms of hypoglycaemia (e.g. tachycardia)

43
Q

Beta-blockers can mask symptoms of thyrotoxicosis. T or F?

A

True.

44
Q

why are beta-blockers used with caution in people with psoriasis?

A

Very rare: beta-blockers may provoke or worsen psoriasis or induce psoriasis-like rash, alopecia.

45
Q

As with other beta-blockers, bisoprolol may increase both the sensitivity towards allergens and the severity of anaphylactic reactions. Adrenaline treatment does not always give the expected therapeutic effect. T or F?

A

True.

46
Q

can a beta-blocker be continued peri-operatively?

A

Yes.
In patients undergoing general anaesthesia, beta-blockade reduces the incidence of arrhythmias and myocardial ischemia during induction and intubation and the post-operative period. It is currently recommended that maintenance beta-blockade be continued peri-operatively. The anaesthesist must be aware of beta-blockade because of the potential for interactions with other drugs, resulting in bradyarrhythmias, attenuation of the reflex tachycardia and the decreased reflex ability to compensate for blood loss. If it is thought necessary to withdraw beta-blocker therapy before surgery, this should be done gradually and completed about 48 hours before anaesthesia.

47
Q

Concomitant use of centrally acting antihypertensive drugs may worsen heart failure by a decrease in the central sympathetic tonus (reduction of heart rate and cardiac output, vasodilation). Abrupt withdrawal, particularly if prior to beta-blocker discontinuation, may increase the risk of “rebound hypertension”. T or F?

A

True.

centrally-acting antihypertensives - clonidine, methyldopa, moxonidine

48
Q

NSAIDs may increase the hypotensive effect of bisoprolol. t or F?

A

False, they decrease the hypotensive effect of the beta-blocker.

49
Q

why are beta-blockers not recommended in pregnancy?

A

they reduce the placental perfusion, which has been associated with intrauterine death, growth retardation and abortion or early labour.

bradycardia and hypoglycaemia may occur in the foetus or the newborn infant

if treatment with beta-blockers is necessary, beta-1-selective adrenoceptor blockers are preferable.

50
Q

constipation and diarrhoea are common side effects with beta-blockers. T or F?

A

True.

51
Q

what are the most common side effects expected with OVERDOSE of a beta-blocker?

A

bradycardia, hypotension, bronchospasm, acute cardiac insufficiency and hypoglycaemia

52
Q

how would you treat bradycardia after an overdose of a beta-blocker?

A

administer IV atropine or isoprenaline (or another agent with positive chronotropic properties) if inadequate response to atropine

53
Q

how would you treat hypotension

A

IV fluids and vasopressors

+ IV glucagon may be useful

54
Q

bisoprolol is hardly dialysable. T or F?

A

true.

55
Q

isoprenaline could be given under what circumstances?

A

1) 2nd or 3rd degree AV block
2) bradycardia - if insufficient response to IV atropine
2) Bronchospasm

56
Q

Bisoprolol can be used in the treatment of hypertension. What is the MoA?

A

MoA not quite understood, however, there is evidence that bisoprolol reduces plasma renin activity markedly.

57
Q

Is bisoprolol cardioselective?

A

Yes, it is a potent highly beta1-selective-adrenoceptor blocking agent, lacking intrinsic stimulating activity. It only shows low affinity to the beta2-receptor of the smooth muscles of bronchi and vessels as well as to the beta2-receptors concerned with metabolic regulation. Therefore, bisoprolol is generally not to be expected to influence the airway resistance and beta2-mediated metabolic effects.

58
Q

bisoprolol has a long half-life (10-12h). T or F?

A

true.

59
Q

bisoprolol has high oral bioavailability (90%). T or F?

A

True.

60
Q

why is a dosage adjustment of bisoprolol not required in liver impairment or renal insufficiency?

A

because 50% of bisoprolol is excreted unmetabolised in the urine and another 50% is metabolised by the liver to inactive metabolites and then excreted by the kidneys.

61
Q

what are the common side effects of beta-blockers?

A

bradycardia, cold extremities, constipation, abdominal discomfort, diarrhoea, confusion, dizziness, depression, dry eye, erectile dysfunction, fatigue, sleep disorders, syncope, dyspnoea, N+V

62
Q

hallucinations are a common side effect of beta-blockers. T or F?

A

False, they are rare.

63
Q

Atrioventricular shock and bronchospasm are uncommon side effects of beta-blockers. T or F?

A

True.

64
Q

what are the maximum recommended single dose and daily dose of carvedilol for the treatment of hypertension?

A

25mg single dose

50mg daily dose

65
Q

what is the max. daily dose of carvedilol for patients with symptomatic HF?

A

Max. 25mg BD for patients under 85kg or with severe HF

Max. 50mg BD in patients over 85kg

66
Q

Hypercholesterolaemia is a common side effect of which beta-blocker?

A

carvedilol

67
Q

What are the common side effects of carvedilol?

A 
anaemia
hyperglycaemia and hypoglycaemia
oedema and pulmonary oedema
asthma
dyspepsia
eye irritation
increased weight
urinary disorders and renal impairment
68
Q

Are dose adjustments of carvedilol required in hepatic impairment?

A

yes - in moderate impairment

avoid carvedilol in severe impairment

69
Q

why should carvedilol be taken with food in HF?

A

The tablets do not need to be taken with a meal. However, it is recommended that heart failure patients take their carvedilol medication with food to allow the absorption to be slower and the risk of orthostatic hypotension to be reduced.

70
Q

what are the C/I for carvedilol?

A

acute or decompensated HF requiring IV inotropes

71
Q

Very rare cases of severe skin reactions, such as toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) have been reported during treatment with carvedilol. T or F?

A

True.

72
Q

Agents with non-selective beta-blocking activity may provoke chest pain in patients with Prinzmetal’s variant angina. T or F?

A

true.

73
Q

which beta-blocker is a substrate and an inhibitor of P-glycoprotein?

A

carvedilol

74
Q

which CYP450 enzymes are involved in the metabolism of carvedilol?

A

CYP2D6 and CYP2C9

75
Q

Fluoxetine is a strong inhibitor of which CYP450 enzyme?

A

CYP2D6

NB: Paroxetine is a strong CYP2D6 inhibitor as well.

76
Q

Concomitant administration of clonidine with agents with beta-blocking properties may potentiate blood-pressure- and heart-rate-lowering effects. Which drug should be discontinued first?

A

stop the beta-blocker first, discontinue clonidine several days later by gradually decreasing the dosage.

77
Q

Carvedilol interacts with amiodarone, which results in:

A

Bradycardia, cardiac arrest, and ventricular fibrillation

78
Q

Agents with beta-blocking properties may enhance the blood sugar reducing effect of insulin and oral hypoglycaemics. T or F?

A

True. Regular monitoring of blood glucose is recommended.

79
Q

Carvedilol should not be used during pregnancy unless the potential benefit outweighs the potential risk. What would you do if carvedilol is used close to delivery?

A

infants should be monitored for signs of alpha-blockade and beta-blockade

80
Q

which beta-blocker may cause urinary incontinence in women which resolves upon discontinuation of the medication?

A

carvedilol

81
Q

which beta-blocker is highly protein-bound?

A

carvedilol

NB: bisoprolol is 30% protein-bound

82
Q

Carvedilol is a racemate of two stereoisomers. Both enantiomers were found to have alpha-adrenergic blocking activity in animal models. Non-selective beta1- and beta2-adrenoceptor blockade is attributed mainly to the S(-) enantiomer. T or F?

A

True.

83
Q

Is carvedilol water-soluble or lipid-soluble?

A

carvedilol is highly lipophilic

84
Q

ow is carvedilol eliminated from the body?

A

Carvedilol is primarily metabolised in the liver to a number of metabolites that are mainly eliminated via bile and faeces.
(NB: This explains why dose adjustments are required in hepatic impairment but there isn’t anything about dose adjustments in renal impairment).

85
Q

should labetalol be taken with or without food?

A

with food

86
Q

Labetalol should be used with caution in liver damage. T or F?

A

True. There have been rare reports of severe hepatocellular injury with labetalol therapy. The hepatic injury is usually reversible and has occurred after both short and long-term treatment.
appropriate lab testing needed at 1st symptom of liver dysfunction - if lab evidence of damage or jaundice -> labetalol should be stopped and not restarted.

87
Q

cimetidine, alcohol and hydralazine may increase the concentration of which beta-blocker?

A

labetalol

88
Q

common side effects of labetalol are:

A

ejaculation failure, drug fever, urinary disorders, hypersensitivity
specific side effects with IV use: fever; hypoglycaemia and thyrotoxicosis masked
specific side effects with oral use: photosensitivity reaction

89
Q

tremor is a rare side effect of labetalol. T or F?

A

True.

NB: COncomitant use of labetalol with TCAs can increase the risk of tremor.

90
Q

which beta-blocker can be used in pregnancy?

A

labetalol
the use of labetalol in maternal hypertension is not known to be harmful, except possibly for the 1st trimester. if labetalol is used close to delivery, infants should be monitored for signs of alpha- and beta-blockade

91
Q

wat is the MoA of labetalol?

A

Labetalol hydrochloride lowers the blood pressure by blocking peripheral arteriolar alpha-adrenoceptors thus reducing peripheral resistance, and by concurrent beta-blockade, protects the heart from reflex sympathetic drive that would otherwise occur.

In patients with angina pectoris co-existing with hypertension, the reduced peripheral resistance decreases myocardial afterload and oxygen demand. All these effects would be expected to benefit hypertensive patients and those with co-existing angina.

92
Q

Only negligible amounts of labetalol cross the BBB in animal studies. T or F?

A

True.

93
Q

Is dose reduction of labetalol required in hepatic and renal impairment?

A

Yes, for both.

Cardiovascular BNF chapter (1 decks)

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