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Clinical Pharmacology > Cardiovascular Pharmacology 💊 > Flashcards

Cardiovascular Pharmacology 💊 Flashcards

1
Q

What are examples of class 1 anti arrhythmic drugs?

A

Lidocaine, flecainide, propafenone

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2
Q

What are examples of class 2 anti arrhythmic drugs?

A

Bisoprolol, metoprolol, propranolol

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3
Q

What are examples of class 3 anti arrhythmic drugs?

A

Amiodarone, sotalol

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4
Q

What are examples of class 4 anti arrhythmic drugs?

A

Verapamil, diltiazem

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5
Q

What what kind of tissue will lidocaine have most of an effect?

A

Fast beating or ischaemic tissue

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6
Q

When are class 1b agents used?

A

In ventricular tachycardia especially during ischaemia

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7
Q

What is the effect of class 1b drugs on an ECG?

A

No difference to normal tissue. It fast beating or ischaemic tissue the QRS will be prolonged

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8
Q

What are the side effects of class 1b anti arrhythmic drugs?

A

Dizziness, drowsiness, abdominal upset

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9
Q

What is automaticity?

A

The ability to spontaneously depolarise and generate an action potential

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10
Q

How do class 1C anti arrhythmics affect an ECG?

A

Increased PR, QRS and QT

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11
Q

Why must IV amiodarone be administered through a central line and not a peripheral cannula?

A

Can cause thrombophlebitis if through peripheral cannula

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12
Q

What is the action of class 1 anti arrhythmics?

A

Sodium channel blockers

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13
Q

What is the action of class 2 anti arrhythmics?

A

Beta blockers- beta adrenergic antagonists

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14
Q

What is the action of class 3 anti arrhythmics?

A

Potassium channel blockers

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15
Q

What is the action of class 4 anti arrhythmics?

A

Calcium channel blockers

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16
Q

How do class 1B drugs affect the fast cardiac action potential in cardiac myocytes?

A

Shorten refractory period and action potential duration

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17
Q

What affect do beta blockers have on slow action potential in SA node?

A

Decreased slope of phase 4 depolarisation and prolonged depolarisation

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18
Q

What effect of beta blockers can be seen on an ECG?

A

Increased PR interval

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19
Q

What effect do class 3 drugs have on action potential in cardiac myocytes?

A

Slow repolarisation so prolong refractory period and action potential duration

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20
Q

What affect do class 4 drugs have on the slow action potential in SA node?

A

Slow rise of action potential and prolong repolarisation- increasing refractory period and increasing PR interval

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21
Q

Why are beta blockers used in atrial fibrillation?

A

They decrease heart rate and promote conversion to sinus rhythm

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22
Q

Why would we use long term oral anti-coagulant therapy in a patient with atrial fibrillation?

A

This reduces the risk of stroke associated with AF

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23
Q

Why would a class 2 or 4 drug be used in AV nodal re-entry (a type of SVT)?

A

These drugs slow conduction through the AV node

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24
Q

Why is it that class 1 anti arrhythmics show greater effects on areas of damaged or fast beating cardiac tissue?

A

They bind more rapidly to open or inactivated Na+ channels so show greater effects in tissues that are frequently depolarising

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25
Q

What is the drug of choice for ventricular arrhythmias, what are other alternatives?

A

Drug of choice is amiodarone however lidocaine and mexiletine can also be used in conjunction with amiodarone

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26
Q

Out of the two class 1B anti arrhythmics which is given orally and which IV?

A

Lidocaine- IV

Mexiletine- orally

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27
Q

What are the therapeutic uses of flecainide?

A

Used in AF in patients without structural heart disease and in refractory ventricular arrhythmias

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28
Q

What are common adverse effects with beta blockers?

A

Bradycardia, hypotension and fatigue

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29
Q

What drugs can prevent life-threatening arrhythmias occurring subsequent to myocardial infarction?

A

Beta-blockers

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30
Q

Which drugs can be used in AF to control rate?

A

Bisoprolol, verapamil, diltiazem

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31
Q

Which drugs can be used in AF for rhythm control?

A

Sotalol, flecainide with bisoprolol, amiodarone

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32
Q

Which IV drugs would you use for ventricular tachycardia?

A

IV metoprolol/ lidocaine or amiodarone

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33
Q

Which drug is best for Wolff Parkinson White syndrome?

A

Flecainide

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34
Q

What are the side effects fo ACEi?

A

Dry cough, hypo tension, hyperkalaemia, angioedema, exacerbation of renal disease

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35
Q

What are some DDIs of ACEi?

A

Caution with other hypotensives and drugs that increase potassium, also with NSAIDs

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36
Q

What are some side effects of angiotensin receptor blockers?

A

Hypotension, hyperkalaemia, exacerbation of renal disease

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37
Q

What is the difference between Phenylalkylamines and dihydropyridine Calcium channel blockers?

A 
Phenylalkylamines are cardio selective and so are used class 4 anti-arrhythmics
Dihydropyridines are used as hypotensives
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38
Q

What are some adverse drug reactions of calcium channel blockers (dihydropyridines)?

A

Hypotension, dizziness, palpitations, ankle swelling and flushing (many side effects are from vasodilation the drug causes)

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39
Q

What are contraindications for using. Calcium channel blocker to treat hypertension?

A

Aortic stenosis, unstable angina

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40
Q

What would the effect be on sim a statin if the patient would taking amlodipine simultaneously?

A

There would be increased effect of the statin as amlodipine is a CYP3A4 inhibitor preventing metabolism of the statin

41
Q

What are some adverse drug reactions of class 4 anti-arrhythmic agents?

A

Heart block, bradycardia, cardiac failure, constipation

42
Q

What are some ADRs of spironolactone?

A

Hyperkalaemia, gynaecomastia

43
Q

What are some contraindications for spironolactone use?

A

Addison’s disease, hyperkalaemia, pregnancy

44
Q

How do alpha blockers head reduce blood pressure?

A

They are antagonists selective to alpha 1 adrenoreceptors found in blood vessels that normally increase sympathetic tone. Therefore they help reduce sympathetic tone

45
Q

What are some ADRs associated with alpha blockers?

A

Dizziness, syncope, headache, fatigue, postural hypotension

46
Q

Why would you try to avoid giving alpha blockers along side dihydropyridines?

A

Both cause peripheral vasodilation so there is a risk of oedema

47
Q

How do beta blockers help reduce blood pressure?

A

Reduce heart rate and contractility and also decrease sympathetic tone of blood vessels

48
Q

What are some ADRs associated with beta blockers?

A

Bronchospasm, heart block, lethargy, impotence

49
Q

What are some contraindications for beta blockers?

A

Asthma, AV node dysfunction, hepatic failure

50
Q

Why would you avoid giving someone with gout a thiazide/thiazide-like diuretic?

A

They have an adverse drug reaction of hyperuricaemia

51
Q

If a patient was over 55 or from a black-African/African-Caribbean ethnicity what would be your first line hypertension treatment?

A

Calcium channel blocker

52
Q

If a patient was under 55 and not from a black-African/African-Caribbean ethnicity what would be your first line hypertension treatment?

A

ACEi or ARB

53
Q

If a patient has hypertension with type 2 diabetes which drug is first line to treat the hypertension?

A

ACEi or ARB

54
Q

What is an example of an alpha-adrenoreceptor blocker?

A

Doxazosin

55
Q

Why are CCBs first line for younger and black African-Caribbean groups?

A

Much less likely to have increased renin

56
Q

Why can spironolactone cause gynaecomastia?

A

Spironolactone reduces androgen activity causing an imbalance in oestrogen to androgen ratio

57
Q

When should a beta or alpha blocker be considered over spironolactone to rest resistant hypertension?

A

When potassium levels are higher than 4.5mmol, due to risk of hyperkalaemia with spironolactone

58
Q

Which of arterial and venous thrombi have higher platelet content?

A

Arterial

59
Q

Which of anti-platelets and anticoagulants work better at preventing venous thrombi?

A

Anticoagulants

Antiplatelets work best for arterial thrombi

60
Q

How does aspirin work as an anti platelet?

A

Inhibits COX-1 mediated production of thromboxane A2 which is a platelet aggregating agent

61
Q

What are some ADRs of aspirin?

A

GI irritation, peptic ulcers, haemorrhage and hypersensitivity

62
Q

What are contraindications to aspirin use?

A

Reye’s syndrome (dont give to under 16s), hypersensitivity and pregnancy (third trimester)

63
Q

When can low dose aspirin be used?

A

AF, secondary prevention of stroke, TIa and acute coronary syndromes, post PCI, after MI

64
Q

What are some examples of ADP receptor antagonists?

A

Clopidogrel, prasugrel and ticagrelor

65
Q

Is clopidogrel a reversible or irreversible inhibitor?

A

Clopidogrel is an irreversible inhibitor

66
Q

Which of ticagrelor and clopidogrel have a faster onset?

A

Ticagrelor has a more rapid onset of action than clopidogrel

67
Q

How does dipyridamole act as an anti-platelet?

A

Phosphodiesterase inhibitor inhibiting GP2b/3a expression

Prevents adenosine re-uptake, increased plasma conc, inhibits platelet aggregation

68
Q

What is an example of a glycoprotein 2b/3a inhibitor?

A

Abciximab

69
Q

What are examples of two fibrinolytic agents?

A

Streptokinase and alteplase

70
Q

Why can streptokinase only be used once?

A

The body develops antibodies to it

71
Q

What drugs works to stop bleeding by inhibiting fibrinolysis?

A

Transexamic acid

72
Q

Why should ACEi be offered to all patients post MI once haemodynamic ally stable?

A

Prevents left ventricular remodelling

73
Q

Why is clopidogrel contraindicated in hepatic failure?

A

Metabolised in liver by CYPs to produce active metabolites

74
Q

Which of the DOACs is a direct thrombin inhibitor?

A

Dabigatran

75
Q

What agents can be used to reverse the defects of warfarin?

A

Vitamin K and prothrombin complex concentrate

76
Q

Which clotting factors production are affected by warfarin as they require vitamin K as a cofactor for activation?

A

2, 7, 9, 10

77
Q

What enzyme does warfarin inhibit?

A

Vitamin K epoxide reductase

78
Q

What drugs can increase the effects of warfarin?

A

CYP2C9 inhibitors, cephalosporins, high protein binding drugs, drugs that decrease Vit K absorption

79
Q

What are some drugs which increase warfarin metabolism and therefore decrease its effects?

A

Barbiturates, phenytoin, rifampicin, St Johns Wort

80
Q

What would a higher INR indicate in regards to how anti coagulated the blood is?

A

High INR= more anti coagulated

81
Q

What are some DOACs which are direct Xa inhibitors?

A

Apixaban, edoxaban, rivaroxaban

82
Q

What are two examples of low molecular weight heparins?

A

Dalteparin, enoxaparin

83
Q

What is fondaparinux?

A

Synthetic pentasaccharide (heparin)

84
Q

How does heparin work as an anticoagulant?

A

Inhibits clotting factor Xa

85
Q

What are some ADRs related to heparin from common to rare?

A

Bruising/bleeding
Heparin induced thrombocytopenia
Hyperkalaemia
Osteoporosis (long term use)

86
Q

What is the reversal agent of heparin?

A

Protamine sulphate

87
Q

What is an example of a cholesterol absorption inhibitor?

A

Ezetimibe

88
Q

Ezetimibe is an inhibitor of what transporter at the brush border?

A

NPC1L1

89
Q

What drug class is alirocumab an example of?

A

PCSK9 inhibitors

90
Q

How do PCSK9 inhibitors help to reduce plasma lipid levels?

A

Prevent LDL receptor degradation

91
Q

What statin (+dose)do we use for primary and secondary prevention of CVD?

A

Primary: 20mg atorvastatin
Secondary: 80mg atorvastatin

92
Q

What enzyme do statins inhibit?

A

HMG-CoA reductase

93
Q

How does simvastatin’s half life compare to atorvastatin’s?

A

Simvastatin has a short half life of around 2 hours

Atorvastatin has a longer half life of around 24 hours

94
Q

What are ADRs associated with statins?

A

GI disruption, nausea, headache, myalgia

Very rarely- rhabdomyolysis

95
Q

What drugs can affect statin effects?

A

Amiodarone, amlodipine, diltiazem, macrolides (these all increase plasma conc of the statin by inhibiting CYP3A4)

96
Q

What is an example of a fibrate used in hyperlipidaemia?

A

Fenofibrate

97
Q

How do vibrates help treat hyperlipidaemia?

A

Activation of PPAR-a gene which increases lipoprotein lipase production

98
Q

What are some ADRs associated with fibrates?

A

Gall stones (cholelithiasis), GI upset are rarely myositis

Clinical Pharmacology (12 decks)

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