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Pre-reg revision > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

Questions from the BNF chapter on the CV system

1
Q

Which is NOT included in the CHADSVAS score?

  • Hypertension
  • Renal Impairment
  • Aged 65-74
  • Diabetes
A

Renal Impairment

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2
Q

Which would score 2 POINTS when calculating the CHADSVAS score?

  • Female gender
  • Age 65-74
  • Previous stroke/TIA/thromboembolism
  • Existing vascular disease including MI/atherosclerosis/peripheral disease
A

Previous stroke/TIA/thromboembolism

The other risks would score one point each

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3
Q

What does the CHADSVASC score measure?

A

Stroke + thromboembolism risk in AF

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4
Q

When would you use the CHADSVASC score?

A

To assess risk of stroke and thromboembolism in AF

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5
Q

What is ‘rate control’ in AF?

A

Where the heart remains in AF but the ventricular heart rate is reduced

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6
Q

What is ‘rhythm control’ in AF?

A

Where the heart is converted back to sinus rhythm either through electrical or pharmacological cardioversion

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7
Q

What should be used for 1st line rate control in AF?

A

Beta-blockers or rate limiting CCBs

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8
Q

Which drug should not be used in rate control of AF?

  • Digoxin
  • Verapamil
  • Amiodarone
  • Propranolol
A

Amiodarone

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9
Q

When is ‘pill in the pocket’ used?

A

Paroxsymal AF

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10
Q

Which drug is the ‘pill in the pocket’ for paroxsymal AF?

A

Flecainide 300mg or Propafenone 600mg

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11
Q

Which antiarrythmic class is flecainide?

A

Class Ic

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12
Q

What score in CHADSVAS means that stroke prevention is indicated?

A

1 or more for men

2 or more for women

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13
Q

Which is NOT included in the HAS-BLED score?

  • abnormal liver function
  • age >65
  • harmful alcohol consumption
  • hypotension
A

Hypotension

uncontrolled hypertension is

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14
Q

‘Anticoagulation should not be withheld solely because of risk of falls’
True or False

A

True

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15
Q

Which is included in the HAS-BLED score?

  • labile INR
  • use of anti-epileptic drugs
  • risk of falls
  • abnormal thyroid function
A

Labile INR

Poorly controlled INR, less than 60% time in range

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16
Q

‘Hypokalaemia can induce long QT syndrome’

True or false?

A

True

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17
Q

‘Verapamil is a positive inotrope’

True or false?

A

False - it is a negative inotrope

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18
Q

‘Anti-arrythmics can never cause arrythmias’

True or false?

A

False - in some circumstances anti-arrythmics can provoke arrythmias

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19
Q

Which calcium channel blocker is licensed for atrial fibrillation?

  • Verapamil
  • Amlodipine
  • Diltiazem
A

Verapamil

Diltiazem can be used but this is an unlicensed treatment

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20
Q

Why should digoxin only be started in sedentary patients?

A

It is only effective at controlling the ventricular rate at rest

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21
Q

What is the aim of rate control in AF?

A

Reduce the ventricular rate to <100

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22
Q

Which is a common side effect of verapamil?

  • constipation
  • vomiting
  • hallucinations
  • anorexia
A

Constipation

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23
Q

When should diltiazem be prescribed by brand?

  • All MR preparations
  • In elderly patients
  • MR preparations containing over 60mg
  • Always
A

MR preparations containing over 60mg.

Different versions of MR preps containing over 60mg may not have the same clinical effect

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24
Q

Which statement is FALSE?

  • Sotalol can prolong the QT interval
  • Sotalol is a selective beta blocker
  • Sotalol is contra-indicated in asthma
  • Sotalol can cause life threatening ventricular arrythmias, particularly in hypokalaemia
A

Sotalol is a selective beta blocker

It is non-selective

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25
Q

Name a class II anti-arrythmic

A

Class II = Beta blockade

propranolol, esmolol, sotalol

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26
Q

Name a class III anti-arrythmic

A 
Class III = K+ channel blockade
amiodarone, sotalol (also class II)
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27
Q

Name a class IV anti-arrythmic

A

Class IV = calcium channel blockade

diltiazem, verapamil

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28
Q

Name a class Ic (strong) anti-arrythmic

A

flecainide, propafenone

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29
Q

Name a class Ia (moderate) anti-arrythmic

A

quinidine

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30
Q

Name a class Ib (weak) anti-arrythmic

A

lidocaine

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31
Q

How do class I anti-arrythmics work?

A

Membrane stabilising drugs

Work via sodium channel blockade

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32
Q

What is the major interaction between verapamil and beta-blockers?

A

Cardiac depressant effects

Risk of asystole, bradycardia and sinus arrest

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33
Q

Which CCB can never be given with beta-blockers

A

Verapamil - risk of cardiac depression

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34
Q

How does digoxin work?

A

Cardiac glycoside

Increases force of myocardial contraction and reduces conductivity in the AV node

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35
Q

What is xanthopsia?

A

Colour vision deficiency - a ‘yellowing’ of vison

Caused by digoxin toxicity

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36
Q

Which drug can cause a yellowing of vision?

A

Digoxin - causes xanthopsia

Sign of digoxin toxicity

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37
Q

Which of these is not a sign of digoxin toxicity?

  • blurred vision / visual disturbances
  • vomiting
  • syncope
  • abdominal pain
A

Syncope - although fatigue and delirium are common signs

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38
Q

‘Digoxin is mainly hepatically cleared’

True or False?

A

False - it is largely eliminated renally

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39
Q

Which of these can contribute to digoxin toxicity?

  • Hypernatraemia
  • Dehydration
  • Hypokalamia
  • Liver disease
A

Hypokalaemia can contribute to digoxin toxicity

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40
Q

Which of these would not be involved in causing digoxin toxicity?

  • AKI
  • Hypokalaemia
  • Use of vitamin D supplements
  • Hypertension
A

Hypertension

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41
Q

Name the four DOACs

A

Rivaroxaban
Apixaban
Edoxaban
Dabigatran

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42
Q

Which is not an indication for an anticoagulant?

  • PE
  • DVT
  • AF
  • HTN
A

HTN

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43
Q

What is the most common side effect of anticoagulants

A

Bleeding/ haemorrhage

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44
Q

What colour is a 1mg warfarin tablet?

A

Brown

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45
Q

What colour is a 3mg warfarin tablet?

A

Blue

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46
Q

What colour is a 5mg warfarin tablet?

A

Pink

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47
Q

What colour is a 500mcg warfarin tablet and why is this not usually stocked?

A

White

Easily confused with other tablets

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48
Q

What is the maximum amount of time that a patient on warfarin can go without having their INR checked?

A

12 weeks

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49
Q

How long does it take for the anticoagulant effect of warfarin to develop?

A

48 to 72 hours

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50
Q

What can be given to reverse the effects of warfarin?

A

Vitamin K (phytomenadione)

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51
Q

In which circumstance would you advise to stop warfarin and give vitamin K by a slow IV injection?

  • INR >8, no bleeding
  • INR 6, minor bleeding
  • INR 5, no bleeding
  • INR 2, minor bleeding
A

INR 6 and minor bleeding

For unexpected bleeding at therapeutic levels you should always investigate the possibilty of underlying causes

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52
Q

In which circumstance would you advise to stop warfarin and give vitamin K injection orally?

  • INR >8, no bleeding
  • INR 6, minor bleeding
  • INR 5, no bleeding
  • INR 2, minor bleeding
A

INR >8 no bleeding

unlicensed use of vitamin K injection
restart warfarin when INR <5

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53
Q

Which drugs interact with digoxin?

  • alfacalcidol
  • ramipril
  • amoxicillin
  • prednisolone
  • salbutamol
A

Alfacalcidol - increased risk of digoxin toxicity. Manufacturer advises monitor.
Prednisolone - increased risk of digoxin toxicity. Manufacturer advises caution.
Salbutamol - increased risk of digoxin toxicity. Manufacturer advises caution.

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54
Q

‘There is an interaction between macrolides and digoxin’

True or false?

A

True - macrolides can cause a 2x to 4x increase in digoxin concentration, advised to monitor digoxin levels

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55
Q

‘Hypokalaemia contributes to digoxin toxicity’

True or False

A

TRUE - monitor for K+ depleting diuretics as this can increase the risk of digoxin toxicity

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56
Q

Which anti-arrythmic class is amiodarone in?

A

Class III

K+ channel blockade

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57
Q

Which system is NOT affected by amiodarone?

  • Skin
  • Renal
  • Thyroid
  • Respiratory
A

Renal

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58
Q

‘Amiodarone has a short half life’

True or false?

A

False
Amiodarone has a long half life and takes several weeks to reach steady state. Because of this, drug interactions can still occur several weeks after treatment cessation

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59
Q

What colour can amiodarone potentially cause skin to become?

A

Slate-grey

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60
Q

Which drug can cause patients to become dazzled by headlights at night?

A

Amiodarone

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61
Q

What effect can amiodarone have on the eyes?

A

Causes corneal microdeposits which can cause patient to be dazzled
Reversible on withdrawal of treatment

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62
Q

How does amiodarone affect the thyroid and what is the reason for this?

A

Can cause disorders in thyroid function - both hyper and hypo.
Because amiodarone contains iodine.
Hyperthyroidism can be permanent and fatal

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63
Q

What monitoring should a patient prescribed amiodarone have?

A

Thyroid function tests at beginning of treatment and every 6 months
Chest x-ray prior to treatment + should be told to report any new/progressive SOB
Liver function tests at beginning of treatment and every 6 months

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64
Q

Which drug does NOT interact with amiodarone

  • warfarin
  • simvastatin
  • lithium
  • ramipril
  • bisoprolol
A

RAMIPRIL

warfarin - inhibited metabolism, increase in anticoagulant effect
simvastatin - increased risk of myopathy
lithium - increased risk of arrythmias
bisoprolol- increased risk of cardiovascular side effects

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65
Q

Why should amiodarone NEVER be given with sofosbuvir/ hep C treatments

A

Risk of severe bradycardia and heart block

MHRA warning

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66
Q

‘Warfarin is teratogenic’

True or false?

A

True - risk of congenital malformations in first trimester

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67
Q

Which vitamin K antagonist can rarely cause calciphylaxis?

A

Warfarin

  • more common in patients with renal disease
  • patients should report any painful skin rash
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68
Q

What is the interaction between St John’s Wort and warfarin?

A

St John’s wort decreases the INR/anticoagulant effect

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69
Q

What is the interaction between fluconazole and warfarin?

A

Fluconazole raises the INR/ increases anticoagulant effect

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70
Q

What is the target concentration/therapeutic range for serum digoxin?

A

1 - 2 mcg/L

Toxicity can occur >2.0 mcg/L

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71
Q

What is the approx time for dioxin to reach steady state?

A

7 days

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72
Q

When should a digoxin level be taken?

A

Pre-dose or 6 - 8 hours post dose

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73
Q

Name two non-dihydropyridine calcium channel blockers

A

Verapamil + diltiazem

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74
Q

What are the advantages of beta blockers with intrinsic sympathomimetic activity?

A

Less coldness to the extremities and bradycardia

can stimulate as well as block adrenergic receptors

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75
Q

Which beta blockers have intrinsic sympathomimetic activity?

A

Celiprolol
Oxprenolol
Pindolol

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76
Q

How do beta blockers work?

A

Block beta-adrenoreceptors in the heart, peripheral vasculature, bronchi, pancreas and liver
They slow the heart rate and depress the myocardium

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77
Q

What are the four most water soluble beta blockers?

A 
Sotalol
Nadolol
Atenolol
Celiprolol
(SNACK without the K)
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78
Q

What are the advantages of water soluble beta blockers?

A

They are less likely to enter the brain and therefore are less likely to cause side effects such as sleep disturbance and nightmares

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79
Q

How are water soluble beta blockers excreted?

A

Via the kidneys

May need dose reductions in renal impairment

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80
Q

‘Most beta blockers have a short duration of action’

True or False?

A

True - they may need to be taken 2 - 3 times per day

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81
Q

Name 4 beta blockers that can be given once daily due to an intrinsically longer duration of action

A 
Atenolol
Bisoprolol
Celiprolol
Nadolol
(ABCN)
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82
Q

Why should beta-blockers be avoided in asthma?

A

Beta blockers can precipitate bronchospasm

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83
Q

Name the cardioselective beta blockers

A 
Atenolol
Bisoprolol
Metoprolol
Nebivolol
Acebutolol
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84
Q

What does the term ‘cardioselective beta blocker’ mean?

A

These beta blockers have less of an effect on the B2 (bronchial) receptors.
They can have a lesser effect on airways resistance and should be used in patients with a history of asthma or COPD.

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85
Q

Which is NOT a side effect of beta blockers?

  • Dry Eyes
  • Hyperkalaemia
  • Cold extremities
  • Syncope
  • Fatigue
A

Syncope

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86
Q

In which condition would a beta-blocker be CONTRAINDICATED?

  • Diabetes
  • Psoriasis
  • Second degree heart block
  • COPD
  • Myasthenia gravis
A

Second degree heart block

Beta-blockers are cautioned in the other listed conditions

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87
Q

Why are beta-blockers cautioned in diabetes?

A
  • They can affect carbohydrate metabolism, causing hyper or hypoglycaemia
  • They can also mask symptoms of hypos such as tachycardia by interfering with metabolic and autonomic responses
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88
Q

‘Abrupt withdrawal of beta-blockers should be avoided’

True or False?

A

True

Esp in ischaemic disease as can cause worsening of myocardial ischaemia

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89
Q

‘Propranolol can be used for anxiety and prophylaxis od migraine’
True or False?

A

True

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90
Q

What serious side effect can occur when beta-blockers are given IV?

A

Excessive bradycardia
Symptoms = dizziness, light headedness and syncope
Can be treated with IV atropine

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91
Q

‘Labetalol is a selective beta blocker’

True or False?

A

False - it is a non-selective alpha and beta blocking drug

92
Q

Can labetalol be used in hepatic impairment?

A

NO - avoid.

Risk of liver damage

93
Q

What monitoring is required for patients taking labetalol?

A

Patients should be monitored for signs of liver damage.
There is a risk of severe hepatocellular damage
LFTs required after first sign of liver dysfunction and stop treatment if there is evidence of any liver damage or jaundice

94
Q

‘Liver damage only occurs in patinets who take labetalol long term’
True or False?

A

False - there is risk of liver damage in short term and long term treatment

95
Q

Can sotalol affect the QT interval?

A

Yes.

Sotalol can prolong the QT interval and cause life-threatening ventricular arrythmias

96
Q

What monitoring is required for a patient taking sotalol?

A

ECG and monitor QT interval

Monitor electrolytes and AVOID/CORRECT hypokalaemia and hypomagnesaemia or any other disturbances

97
Q

Name the 2 non-dihydropyridine CCBs

A

Verapamil and diltiazem

98
Q

What is the most common side effect of verapamil?

A

Constipation

99
Q

Name some dihydropyridine CCBs

A

Amlodipine, felodipine, nifedipine, lercanidipine, nicardipine

100
Q

How do dihydropyridine CCBs work?

A

Relax vascular smooth muscle and dilate coronary and peripheral arteries

101
Q

‘Dihydropyridine CCBs have anti-arrythmic activity’

True or False?

A

False

102
Q

Which dihydropyridine CCBs have a long duration of action and can be given once daily?

A

Amlodipine + felodipine

103
Q

‘Side effects of dihydropyridine CCBs are mainly to do with vasodilation’
True or False?

A

True

Flushing, headache and ankle swelling are common

104
Q

Can calcium channel blockers cause ankle swelling?

A

Yes

105
Q

What would IV Nicardipine be used to treat?

A

Acute life-threatening hypertension

106
Q

How do dihydropyridine CCBs work?

A
  • Interfere with inward displacement of calcium ions through slow channels of active cell membranes
  • Influence myocardial cells, cells in the conducting system of the heart and vascular smooth muscle cells
  • Can reduce myocardial contractility, depress electrical impulses and diminish vascular tone
107
Q

Dihydropyridine CCBs rarely precipitate heart failure, why is this?

A

Because the negative inotropic effect (depression of electrical impulses) is offset but reduction in left ventricular work

108
Q

Which is NOT a sign of calcium channel blocker overdose?

  • Hyperglycaemia
  • Coma
  • Confusion
  • Angioedema
  • Agitation
A

Angioedema

109
Q

‘All preparations of nifedipine must be prescribed by brand’
True or False?

A

False - only MR preps should be prescribed by brand

110
Q

Which brands of Nifedipine must be avoided in oesophageal/GI obstruction, hepatic impairment + IBD?

A

Adalat LA and Valni XL

111
Q

What is normal blood pressure?

A

120/80

112
Q

What is classed as ‘stage 1’ hypertension

A

BP >140/90 clinic or >135/85 home/ambulatory

113
Q

‘Verapamil and diltiazem must be avoided in heart failure’

True or False?

A

True - can cause depression of cardiac function and clinical deterioration

114
Q

Which patient would NOT be treated for stage 1 hypertension?

  • 52 y/o with angina and BP 150/91
  • 48 y/o with CKD stage 3 and BP 141/96
  • 79 y/o with no co-morbidities and BP 145/87
  • 66 y/o with T2DM and BP 140/90
A
  • 79 y/o with no co-morbidities and BP 145/87

Patient has hypertension but is <80 with no risk factors

115
Q

What is classed as stage 2 hypertension?

A

BP >160/100 clinic or 150/95 at home

116
Q

Which patients with stage 2 hypertension would receive treatment with anti-hypertensives?

A

Every patient with stage 2 hypertension would recieve treatment

117
Q

What would be the target blood pressure for a 91 year old patient receiving anti-hypertensives?

A

<150/90 clinic or <145/85 home

For all patients over 80

118
Q

What would be target blood pressure for a 49 year old patient receiving anti-hypertensives?

A

<140/90 clinic or <135/85 home

For patients under 80 with no co-morbidities

119
Q

What is the target blood pressure for patients receiving anti-hypertensives with cardiovascular disease or diabetes with eye, kidney or CVD?

A

<130/80

120
Q

When using a stepwise approach to hypertension, how long should be left between steps to determine response?

A

4 weeks

121
Q

What is the stepwise approach for hypertension for patients under 55?

A
  1. ACEi/ARB (if not tolerated give beta-blocker)
  2. Add CCB
  3. Add thiazide-like diuretic
  4. Add low dose spironolactone or alpha/beta blocker if diuretics not tolerated
122
Q

What is the stepwise approach for hypertension for patients over 55 or with African or Carribean family origin?

A
  1. CCB (if not tolerated/HF give thiazide-like diuretic)
  2. Add ACEi/ARB
  3. Add thiazide-like diuretic
  4. Add low dose spironolactone or alpha/beta blocker if diuretics not tolerated
123
Q

ACEi or ARB?

Which is preferred in patients of African/Carribean heritage?

A

ARB

124
Q

Should aspirin be prescribed for patients with uncontrolled hypertension?

A

No, only for secondary prevention in cardiovascular disease

125
Q

What causes a dry cough with ACEi?

A

Build up of braydkinin

126
Q

Which is not a side effect of ACEi?

  • Taste disturbances
  • Angioedema
  • Profound hypotension
  • Agitation
  • Pancreatitis
A

Agitation

127
Q

What monitoring is required for patients receiving ACEi?

A

Renal function and electrolytes should be monitored before treatment, before dose adjustments and during treatment

128
Q

‘ACEi can have hepatic effects’

True or False?

A

True - there is a risk of choleostatic jaundice, hepatitis and hepatic failure.
Treatment should be discontinued if there is a marked elevation of hepatic enzymes or evidence of jaundice

129
Q

Why should an ACEi and ARB not be used together?

A

There is an increased risk of hypotension, hyperkalaemia and renal impairment

130
Q

Which is not a side effect of ARBs?

  • Angioedema (w delayed onset)
  • Hyperkalaemia
  • Dry cough
  • Symptomatic hypotension
A

Dry cough

131
Q

Name some ARBs

A

Candesartan, Losartan, Irbesartan, Valsartan, Telmisartan

132
Q

What is diuresis?

A

Increased or excessive urine

133
Q

How do thiazide + related diuretics work?

A

Inhibit sodium re-absorption at the beginning of the distal convoluted tubule

134
Q

How quickly do thiazide + related diuretics work?

A

Act within 1-2 hours of administration

135
Q

How long is the duration of action thiazide + related diuretics?

A

12 - 24 hours

136
Q

What time of day should thiazide + related diuretics be administered?

A

Early so diuresis does not interrupt sleep

137
Q

‘Thiazide + related diuretics are generally ineffective if eGFR <30’
True or False?

A

True - except metolazone

138
Q

Why are low-dose thiazide + related diuretics recommended for the treatment of hypertension?

A

Lower doses produce maximal BP-lowering effects with less biochemical disturbance
Lower doses - vasodilation more prominent than diuresis

139
Q

Which types of diuretics can cause hypokalaemia?

A

Thiazide + related diuretics and loop

140
Q

Which thiazide + related diuretic has a long duration of action?

A

Chlortalidone

Useful if rapid diuresis causes acute retention or if patients dislike altered urination

141
Q

What are some problems with diuretics that cause hypokalaemia?

A

In hepatic failure hypokalaemia can precipitate encephalopathy/coma
Hypokalaemia is also dangerous in patients with severe cardiovascular disease

142
Q

‘Thiazide + related diuretics are cautioned in diabetes as they can excerbate this condition and cause hyperglyceaemia’
True or False?

A

True.
Loop diuretics also have this effect but hyperglycaemia is more likely with thiazide + related diuretics.
Indapamide is associated with less metabolic disturbance including less aggrivation of diabetes.

143
Q

Which thiazide + related diuretic can be combined with a loop diuretic to give profound diuresis?

A

Metolazone.

Even effective when eGFR <30 but risk of excessive diuresis, patient requires careful monitoring

144
Q

Why can loop diuretics not be used in patients with enlarged prostates?

A

Risk of urinary retention

145
Q

How quickly do loop diuretics act?

A

Within 1 hour of oral administration.

IV furosemide has a peak of 30 mins

146
Q

What is the duration of action for loop diuretics?

A

Diuresis complete within 6 hours. Suitable for BD dosing without interrupting sleep

147
Q

‘The diuresis associated with loop diuretics is dose-related’
True or False?

A

True

148
Q

How is diuretic-resistant oedema treated?

A

Loop diuretic combined with bendroflumethiazide or metolazone

149
Q

How is furosemide administered IV?

A

Max rate of 4mg/min

150
Q

What are the risks of giving furosemide IV?

A

Can cause ototoxicity (tinnitus and deafness) if administered too quickly

151
Q

When are weak diuretics amiloride+ triamterene used?

A

Given with thiazidelike or loop diuretics as a more effective alternative to potassium supplements.
Act as weak diuretics that cause potassium retention

152
Q

Potassium-sparing diuretics should never be given with … ?

A

Potassium supplements

ACEi / ARBs - risk of severe hyperkalaemia

153
Q

‘Aldosterone antagonists are potassium sparing’

True or False?

A

True - contraindicated in hyperkalaemia

154
Q

Why should diuretics be used with caution in the elderly?

A

They are particularly susceptible to side effects. Low doses should be used initially then adjusted according to renal function

155
Q

‘Brinzolamide and dorzolamide are diuretics’

True or false?

A

True - they inhibit the formation of aqueous humour

156
Q

Why are heparins less useful in preventing thromboembolism in arteries?

A

They are faster flowing vessels, thrombi are formed of less fibrin

157
Q

Why is heparin preferred to LMWH where there is a high bleeding risk?

A

Heparin has a short duration of action therefore the effect can be terminated rapidly when the infusion is stopped

158
Q

What is the reversal agent for heparin?

A

Protamine sulfate

159
Q

Name the LMWHs

A

Dalteparin
Enoxaparin
Tinzaparin

160
Q

Why are LWMH preferred to heparin in the prevention and treatment of VTE?

A
  • Lower risk of heparin-induced thrombocytopenia

- Longer duration of action - once daily dosing is possible

161
Q

Which LMWHs are licensed for extended treatment and prophylaxis of VTE in patients with solid tumours?

A

Dalteparin and Tinzaparin

162
Q

What are the 3 main side effects of heparin?

A

Haemorrhage
Heparin-induced thrombocytopenia
Hyperkalaemia

163
Q

What are the signs of heparin-induced thrombocytopenia?

A
  • 30% reduction in platelet count
  • Thrombosis
  • Skin allergy
164
Q

Why does heparin cause hyperkalaemia?

A

Inhibits aldosterone secretion

165
Q

Which patient would NOT be at higher risk for hyperkalaemia caused by LMWH?

  • CKD stage 4
  • Diabetic
  • Receiving IV antibiotics
  • Taking regular spironolactone
A

Patient receiving IV antibiotics

166
Q

When might factor Xa levels be monitored in a patient receiving LMWH?

A

If they are renally impaired or over or under weight

167
Q

Which of these does NOT increase risk of VTE?

  • Hepatic impairment
  • Age >60
  • Obesity
  • Malignant disease
  • Reduced mobility
A

Hepatic impairment

168
Q

‘Pharmacological prophylaxis should start within 14 hours of admission’
True or False?

A

True

169
Q

Which DOAC can be used for oral treatment and prophylaxis of VTE?

A

Edoxaban

170
Q

In the diagnosis of heart failure what is the range/significance of the N-terminal proBNP level?

A

Suspect a diagnosis of heart failure if the N-terminal pro BNP level is 400-2000ng/L
If the level is <400 then HF is unlikely
A high level can also indicate AF

171
Q

What are some non-pharmacological treatments for heart failure?

A
  • Exercise based rehab
  • Smoking cessation
  • Reduced alcohol intake
172
Q

Name the New York Heart association classification of HF symptoms

A

Class I - no limitations on exercise
Class II - slight limitation of physical activity
Class III - marked limitation of physical activity
Class IV - symptoms of heart failure present at rest

173
Q

‘Verapamil and diltiazem should never be used in heart failure’
True or False?

A

True - the negative inotropic action can further depress cardiac function and cause clinically significant deterioration

174
Q

What are the aims of treatment in heart failure?

A
  • Relieve symptoms
  • Improve exercise tolerance
  • Reduce acute exacerbations
  • Reduce mortality
175
Q

Which two treatments should always be initiated in HF with LVSD?

A
  • ACEi

- Beta blocker

176
Q

Which ARBs are licensed in heart failure?

A

Candesartan, losartan and valsartan

177
Q

Which beta blockers are licensed in heart failure?

A

Bisoprolol, carvedilol, nebivolol (in over 70s with mild HF)

178
Q

‘In heart failure beta blockers should follow the start low and go slow rule’
True or false

A

True
They should be titrated slowly and heart rate, blood pressure and clinical status should be monitored following each dose increase

179
Q

‘Beta blockers may initially cause a deterioration in symptoms when initiated in heart failure’
True or false?

A

True

180
Q

Which MRA is usually started in heart failure?

A

MRA = mineralcorticoid receptor antagonist

Spironolactone 25-50mg OD

181
Q

‘Spironolactone does not affect mortality when used in heart failure’
True or false?

A

False - it can reduce mortality

182
Q

Which criteria must be met for specialist treatment with ivabradine for heart failure?

A

HF with LVSD,
NYHA class II-IV symptoms,
Treatment with ACEi, B blocker and MRA,
Heart rate over 75 BPM

183
Q

What is the minimum resting heart rate that a patient taking ivabradine should be maintained at?

A

Resting heart rate should be above 50bpm

184
Q

Patients taking ivabradine should be monitored for ….

A

Bradycardia and AF

185
Q

What is sacubitral?

A

Neprilysin inhibitor, used with valsartan in specialist treatment of heart failure

186
Q

Does digoxin reduce mortality in heart failure?

A

No but can improve symptoms and reduce hospitalisation

187
Q

When should digoxin be used in heart failure?

A

Specialist use only

In worsening/severe HF with LVSD that remains symptomatic with all other treatments

188
Q

How regularly should patients with heart failure be monitored?

A

Minimum of every 6 months.

Monitor at shorter intervals (days to 2 weeks) if clinical condition or drug treatment changes

189
Q

Which is not included in the QRISK2 score calculator?

  • Diabetes status
  • Systolic BP
  • BMI
  • Diet
  • Severe mental illness
A

Diet

190
Q

Which drugs can cause dyslipidaemia as a side effect and so are included in the QRISK2 calculator?

A
  • Antipsychotics
  • Corticosteroids
  • Immunosuppressants
191
Q

Can a diagnosis of erectile dysfunction increase your risk of heart disease/stroke?

A

Yes

192
Q

‘Cardiovascular risk is underestimated in patients taking antihypertensive drugs’
True or false?

A

True

193
Q

How are statins categorised?

A

In terms of % reduction in LDL-cholesterol levels

  • low intensity is 20-30% reduction
  • medium intensity is 30-40% reduction
  • high intensity is >40% reduction
194
Q

Which is an example of high-intensity statin therapy?

  • Atorvastatin 20mg
  • Simvastatin 10mg
  • Fluvastatin 80mg
A

Atorvastatin 20mg

195
Q

Which is an example of medium-intensity statin therapy?

  • Atorvastatin 40mg
  • Rosuvastatin 5mg
  • Pravastatin 40mg
A

Rosuvastatin 5mg

Pravastatin is always low-intensity therapy

196
Q

How should a QRISK2 score of over 10% be treated?

A

High-intensity statin eg, atorvastatin 80mg

197
Q

Why is simvastatin 80mg not recommended?

A

MHRA found increased risk of myopathy with high dose simvastatin.

198
Q

How is statin therapy monitored?

A

Total cholesterol, HDL and non-HDL cholesterol should be monitored before treatment and 3 months into treatment.
Aiming for >40% reduction in non-HDL cholesterol

199
Q

Why is it important to correct hypothyroidism before initiating a statin?

A

Correcting hypothyroidism may resolve the lipid abnormality and untreated hypothyroidism has an increased risk of myositis with lipid regulating drugs

200
Q

‘Statins reduce cardiovascular disease and total mortality irrespective of initial cholesterol concentration’
True or False?

A

True

They are also more effective than other lipid-regulating drugs at reducing LDL-cholesterol concentration

201
Q

‘Statins are more effective than fibrates are reducing triglyceride concentration’
True or false?

A

False

202
Q

How do bile acid sequestrants such as cholestyramine work?

A

Bind to bile acids and prevent reabsorption, promoting hepatic conversion of cholesterol into bile acid

203
Q

What counselling should be given with bile acid sequestrants?

A
  • They can interfere with the absorption of fat soluble vitamins
  • They can affect absorption of other drugs so should be taken 1 hour prior or 4-6 hours after other drugs
204
Q

Which drug that inhibits intestinal absorption of cholesterol can be given if a statin is not tolerated?

A

Ezetimibe 10mg OD

205
Q

How do statins work?

A

Competitively inhibit HMG CoA reductase, an enzyme involved in cholesterol synthesis especially in the liver

206
Q

Which patients are at increased risk of muscle toxicity caused by statins?

A
  • Personal/family history of muscle disorders
  • High alcohol intake
  • Renal impairment
  • Hypothyroidism
207
Q

How is baseline creatinine kinase used when monitoring statin treatment?

A

Statins should be avoided if creatinine kinase is persistently five times the upper limit of normal

208
Q

In patients with diabetes taking a statin how should HbA1c be measured?

A

Before treatment and 3 months after initiation as risk of hyperglycaemia
Do not discontinue statin if HbA1c is increased as benefits outweigh risks

209
Q

Can statins be taken in pregnancy?

A

No.
Risk of congential abnormalities and decreased cholesterol synthesis can affect foetal development.
Use adequate contraception during treatment and discontinue 3 months before trying to get pregnant.

210
Q

How should patients taking statins be counselled?

A

Report any muscle pains, tenderness or weakness

211
Q

How should liver function be monitored in patients taking statins?

A

Monitor before treatment and at 3 and 12 months.
More frequently if signs of hepatotoxicity.
Avoid in active liver disease and use with caution if history of liver disease.

212
Q

Why should most lipid-regulating medicines be taken at night?

A

Cholsterol levels are highest at night and this allows the drugs to work best

213
Q

Which statins do NOT need to be taken at night?

A

Atorvastatin and Rosuvastatin

Have a longer duration of action and can also be taken in the morning

214
Q

What is first line treatment for stable angina?

A
  1. Sublingual GTN - take before activities known to trigger an attack
  2. B-blocker or (rate-limting) CCB titrated to max. tolerated dose
215
Q

What therapy can be added in patients with stable angina who cannot tolerate a CCB or B-blocker?

A

Monotherapy with:

  • long acting nitrate
  • Ivabradine
  • Nicorandil
  • Ranolazine
216
Q

Why should patients taking ivabradine be monitored for bradycardia and AF?

A

It lowers heart rate through action on the sinus node.

Discontinue if HR is persistently below 50bpm

217
Q

‘Ivabradine is a black triangle drug’

True or false?

A

True

218
Q

‘Nicorandil can cause serous ulceration’

True or false?

A

True - including GI ulcers which may perforate. Stop treatment if ulceration occurs

219
Q

Name some cautions for ranolazine?

A

Weight <60kg, eGFR <80ml/min (avoid if <30), elderly, QT interval prolongation

220
Q

How do nitrates work?

A

They are potent coronary vasodilators

Also reduce venous return meaning reduction in left ventricular work

221
Q

Some common side effects of nitrates?

A
  • Flushing
  • Headache
  • Postural hypotension
222
Q

NItrates are cautioned in patients with ‘tolerance’. How can tolerance be reduced with different nitrate preparations?

A

Transdermal patches - leave off for 8-12 hours/day
MR isosorbide dinitrate + isosorbide mononitrate - Give the 2nd of 2 daily doses after 8 hours not 12
MR isosorbide mononitrate - give OD

223
Q

How long do the effects of sublingual GTN last?

A

20-30 mins

224
Q

When does the ‘POM’ restriction not apply to adrenaline?

A

When 1mg of 1 in 1000 adrenaline is used for emergency treatment of anaphylaxis

225
Q

Which drugs are used in the long term management of ACS?

A 
- Dual antiplatelet
 Aspirin + clopidogrel/ticagrelor/prasugrel for 12 months
- B-blocker
- ACEi
- Statin
- Nitrate (if angina/MI)
- Eplenerone (if MI in HF)

Pre-reg revision (14 decks)

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