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Drug Formulary Y3 > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Name two types of loop diuretics?

A
  1. Furosemide

2. Bumetanide

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2
Q

What are the mechanisms of action of loop diuretics?

A
  1. They act principally on the loop of Henle, inhibiting the Na+/K+/2Cl- co-transporter. As the co-transporter is inhibited, ions and water cannot be reabsorbed into the epithelial cells, and remain in the tubular lumen. They are then excreted in urine.
  2. Loop diuretics have a direct effect on blood vessels, causing dilatation of capacitance veins.
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3
Q

When a patient has acute heart failure, what is the benefit of loop diuretics causing dilatation of veins?

A

In acute heart failure, this reduces preload and improves contractile function of the overstretched heart muscle. This is the primary benefit of loop diuretics in heart failure.

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4
Q

What are the indications for use of a loop diuretic? (3)

A
  1. Relief of breathlessness in acute pulmonary oedema (in conjunction with oxygen and nitrates)
  2. Heart failure - symptomatic treatment of fluid overload
  3. Oedematous states - symptomatic treatment of fluid overload, caused by renal disease or liver failure
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5
Q

What are the contra-indications/warnings for use of loop diuretics? (4)

A
  1. Should not be used in patients with severe hypovolaemia or dehydration.
  2. Should be used in caution in patients at risk of hepatic encephalopathy.
  3. Should not be used in those with severe hypokalaemia or hyponatraemia
  4. They can worsen gout if taken chronically as loop diuretics inhibit uric acid excretion
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6
Q

What are the possible common side effects of using loop diuretics?

A

Possible risk of dehydration and hypotension, as well as low electrolyte states.

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7
Q

If a loop diuretic is taken in high doses, how can it affect hearing?

A

A similar co-transporter found in the ear can also be affected. This co-transporter regulates endolymph composition in the inner ear, and if inhibited can lead to hearing loss and tinnitus.

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8
Q

What are the possible drug interactions for loop diuretics? (3)

A
  1. Potential for loop diuretics to affect drugs that are excreted by the kidneys. Examples include lithium being increased as there is reduced excretion.
  2. Digoxin toxicity may be increased due to diuretic associated hypokalaemia
  3. Can increase ototoxicity and nephrotoxicity of aminoglycosides
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9
Q

Why is bumetanide sometimes preferable for use over furosemide?

A

Bumetanide has a more predictable bioavailability, compared to furosemide whose absorption in the gut is highly variable between individuals and dependent upon gut wall oedema.

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10
Q

Name 3 thiazide/thiazide-like diuretics?

A
  1. Bendroflumethiazide
  2. Indapamide
  3. Chlortalidone
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11
Q

Which co-transporter do thiazides inhibit, and where is it found?

A

Thiazides inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron

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12
Q

What are the indications for use of thiazides? (1)

A
  1. Alternative first-line treatment for hypertension OR as an add-on treatment for hypertension
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13
Q

When are thiazides an alternative first-line treatment for hypertension?

A

Where a calcium-channel blocker would otherwise be used, but is unsuitable- usually due to patient having heart failure.

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14
Q

When is a thiazide used as an add-on treatment for hypertension?

A

When blood pressure is not adequately controlled by a calcium channel blocker PLUS an ACE inhibitor or ARB.

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15
Q

What are the contra-indications for using a thiazide? (2)

A
  1. They should be avoided in patients with hypokalaemia or hyponatraemia
  2. They should be avoided in patients with gout/or who are prone to gout.
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16
Q

What are the potential side effects of using thiazides? (3)

A
  1. Cardiac arrhythmias
  2. May increase plasma concentrations of glucose (unmasking type 2 diabetes), LDL-cholesterol and triglycerides.
    * however their net effect on CV risk is protective.
  3. May cause impotence in men
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17
Q

Why can thiazide cause a side effect of cardiac arrhythmias?

A

As there is increased sodium in the distal tubule, it can be exchanged for potassium, hence increased urinary potassium losses leading to hypokalaemia. This can in turn cause cardiac arrhythmias.

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18
Q

What are the possible drug interactions when using thiazides?

A

The effectiveness of thiazides may be reduced by NSAIDs. If thiazides are used in combination with loop diuretics, electrolyte monitoring is essential.

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19
Q

In relation to potassium levels, why is it beneficial for thiazides to be used alongside ACE inhibitors?

A

Thiazides can cause hypokalaemia, whereas ACE inhibitors can cause hyperkalaemia, and so using both helps to maintain a neutral potassium balance.

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20
Q

Name 2 potassium-sparing diuretics?

A
  1. Amiloride (used as co-amilofruse or co-amilozide)

2. Spironolactone

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21
Q

What is the mechanism of action of potassium-sparing diuretics?

A

They act on the distal convoluted tubule, inhibiting the reabsorption of sodium (and therefore water) by epithelium sodium channels (ENaC), leading to sodium and water excretion, and retention of potassium. Spironolactone acts slightly differently as an aldosterone antagonist, but still has a potassium sparing effect.

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22
Q

What is the indication of use, for potassium sparing diuretics?

A

As part of a combination therapy, for the treatment of hypokalaemia arising from loop- or thiazide- diuretic use.

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23
Q

What are the contra-indications for use of a potassium-sparing diuretic? (2)

A
  1. Avoid in severe renal impairment

2. Hyperkalaemia

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24
Q

What are the potential side effects of using potassium sparing diuretics?

A

Side effects are uncommon in low doses however:

  1. GI upset
  2. Dizziness/hypotension if used in combination with other diuretics
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25
Q

What role does aldosterone play in the absorption of sodium and water in the kidneys? And what role does Amiloride and Spironolactone play in this?

A

Aldosterone stimulates sodium and water absorption in the distal tubule by activating epithelial sodium channels (ENaC). Amiloride directly inhibits ENaC, and spironolactone blocks aldosterone receptors.

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26
Q

Name 4 beta blockers?

A
  1. Atenolol
  2. Bisoprolol
  3. Propanolol
  4. Metoprolol
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27
Q

Which beta-adrenoreceptors are located mainly in the heart?

A

Beta1-adrenoreceptors

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28
Q

Where are B2-adrenoreceptors mainly located?

A

Mostly in smooth muscles of blood vessels and in the airways

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29
Q

What effect do beta-blockers have on beta1-reeptors, and how is this beneficial for the heart?

A

They reduce force of contraction and speed of conduction in the heart, relieving myocardial ischaemia by reducing cardiac work and oxygen demand, thus increasing myocardial perfusion.

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30
Q

How do beta-blockers improve prognosis in heart failure?

A

They play a protective role in terms of the effects of chronic sympathetic stimulation.

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31
Q

How do beta-blockers slow the ventricular rate in atrial fibrillation?

A

They prolong the refractory period of the AV node.

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32
Q

What are the indications for use of beta-blockers? (5) - though 4 first-line

A
  1. Ischaemic heart disease: first-line option to improve symptoms and prognosis associated with angina and coronary artery syndrome.
  2. Chronic heart failure
  3. Atrial fibrillation
  4. Supraventricular tachycardia (SVT) - restores sinus rhythm
  5. Hypertension - not first line! they may be used when other medications are insufficient or inappropriate
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33
Q

How do beta-blockers help lower blood pressure?

A

They work through a variety of means, one of which is reducing renin secretion from the kidneys

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34
Q

What are the contra-indications for beta-blockers? (2 contraindications and 1 warning)

A
  1. Asthma - beta-blockers can cause life threatening bronchospasm
  2. Heart block
  3. COPD - although they can be used, it is prudent to prescribe a beta-blocker that is beta1-selective e.g. atenolol, bisoprolol or metoprolol, rather than non-selective propranolol.
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35
Q

Name 4 calcium-channel blockers?

A
  1. Amlodipine
  2. Nifedipine
  3. Diltiazem
  4. Verapamil
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36
Q

What are the indications for use of calcium-channel blockers? (3)

A
  1. Hypertension
  2. Stable angina
  3. Supraventricular arrhythmia
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37
Q

Which calcium-channel blockers are used for first-line treatment/second-line treatment of hypertension? (2)

A
  1. Amlodipine

2. Nifedipine

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38
Q

Which calcium-channel blockers can be used to treat stable angina? - and which drug is the main alternative?

A

All of them can be used, and beta-blockers are the main alternative.

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39
Q

Which calcium-channel blockers are used to treat supraventricular arrhythmias? (2)

A
  1. Diltiazem

2. Verapamil

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40
Q

What are the effects of decreasing calcium entry into vascular and cardiac cells?

A

It causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure. In the heart, it reduces myocardial contractility.

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41
Q

How do calcium-channel blockers prevent angina?

A

They suppress cardiac conduction, particularly across the AV node, thus slowing ventricular rate. This reduction in cardiac rate, as well as the reduction in contractility and afterload, means there is less myocardial oxygen demand, thus preventing angina.

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42
Q

What are the two classes that calcium-channel blockers can be divided in to?

A
  1. Dihydropyridines

2. Non-dihydropyridines

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43
Q

Which two calcium-channel blockers are dihydropyridines?

A
  1. Amlodipine

2. Nifedipine

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44
Q

Which two calcium-channel blockers are non-dihydropyridines?

A
  1. Diltiazem

2. Verapamil

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45
Q

Which group is more selective for the vasculature as opposed to the heart?

A

The dihydropyridines; amlodipine and nifedipine

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46
Q

Which group are therefore more cardiac selective?

A

The non-dihydropyridines: diltiazem and verapamil

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47
Q

Which of the non-dihydropyridines is most cardiac selective?

A

Verapamil

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48
Q

Which type of calcium-channel blocker should not be prescribed in combination with beta-blockers? (unless under close specialist supervision)

A

Non-dihydropyridines - diltiazem and verapamil

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49
Q

In patients with unstable angina, which calcium-channel blockers should be avoided?

A

Dihydropyridines - amlodipine and nifedipine

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50
Q

Why should dihydropyridines be avoided in patients with unstable angina?

A

Because vasodilation causes a reflex increase in contractility and tachycardia, which increases myocardial oxygen demand.

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51
Q

In patients with severe aortic stenosis, which calcium-channel blockers should be avoided, and why?

A

Dihydropyridines - because they can provoke collapse.

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52
Q

What are the common adverse effects of using amlodipine or nifedipine? (dihydropyridines) (4)

A
  1. Ankle swelling
  2. Flushing
  3. Headache
  4. Palpitations
    - all caused by vasodilation and compensatory tachycardia
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53
Q

What side effects can verapamil cause? (1 common, 3 rare but serious)

A
  1. Constipation (common)
  2. Bradycardia
  3. Heart block
  4. Cardiac failure
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54
Q

Why can diltiazem cause any/all of the side effects associated with calcium-channel blockers?

A

As diltiazem has mixed vascular and cardiac actions.

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55
Q

Name 3 angiotensin-converting enzyme (ACE) inhibitors?

A
  1. Ramipril
  2. Lisinopril
  3. Perindopril
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56
Q

Name the 4 indications for use of an ACE inhibitor?

A
  1. Hypertension - for the first- or second- line treatment, to reduce risk of stroke, mI and death from CVD.
  2. Chronic heart failure - first-line treatment of all grades of heart failure
  3. Ischaemic heart disease - to reduce the risk of subsequent cardiovascular events such as MI and stroke.
  4. Diabetic nephropathy/CKD with proteinuria: to reduce proteinuria and progression of nephropathy. (If prescribed for CKD; need to be low dose and monitored closely).
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57
Q

What is the mechanism of action of ACE inhibitors?

A

ACE inhibitors block the action of the angiotensin-converting enzyme, to prevent the conversion of angiotensin I to angiotensin II. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion. Blocking this pathway reduces peripheral vascular resistance (afterload), which lowers blood pressure.

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58
Q

How do ACE inhibitors slow the progression of CKD?

A

They dilate the efferent glomerular arteriole, which reduces intraglomerular pressure, thus slowing the progression of CKD

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59
Q

How do ACE inhibitors have a beneficial effect in heart failure?

A

As ACE inhibitors block the stimulation of aldosterone, sodium and water excretion is promoted, as they are not reabsorbed. This helps to reduce venous return (preload),

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60
Q

What side effects do ACE inhibitors cause?

4 common and 1 rare

A
  1. Commonly hypotension (after the first dose in particular)
  2. Persistent dry cough (due to increased levels of bradykinin, which is usually inactivated by ACE).
  3. Hyperkalaemia (because a low aldosterone level promotes potassium retention).
  4. Cause/worsen renal failure (particularly relevant in patients with renal artery stenosis)
  5. Angioedema/anaphylactoid reactions (rare)
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61
Q

When should use of ACE inhibitors be avoided? (2)

A
  1. Patients with renal artery stenosis or AKI

2. Women who are/could become pregnant, and those who are breastfeeding.

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62
Q

What are the possible drug interactions when taking ACE inhibitors? (3)

A
  1. Caution needs to be taken when prescribing ACE inhibitors if other potassium elevating drugs are being taken; IV/oral potassium supplements or potassium sparing diuretics.
  2. Taking ACE inhibitors with any diuretic may cause profound first-dose hypotension.
  3. The combination of an NSAID with an ACE inhibitor increases the risk of renal failure.
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63
Q

What is an ARB? (aka AT1 blockers)

A

Angiotensin receptor blocker

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64
Q

Name 3 ARBs?

A
  1. Losartan
  2. Candesartan
  3. Irbesartan
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65
Q

What is the mechanism of action of ARBs?

A

ARBs have a similar effect to ACE inhibitor, but instead of inhibiting the conversion of angiotensin I to angiotensin II, ARBs block the action of angiotensin II on the AT1 receptor.

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66
Q

What are the indications for use of ARBs? (4)

A
  1. Hypertension
  2. Chronic heart failure
  3. Ischaemic heart disease
  4. Diabetic neuropathy/CKD with proteinuria
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67
Q

Why are ARBs sometimes prescribed instead of ACE inhibitors, if ACE inhibitors are cheaper and have the same indications for use?

A

ARBs are less likely to cause a dry cough, as they do not inhibit ACE, and therefore do not affect bradykinin metabolism. For the same reasons, they are less likely to cause angioedema too.

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68
Q

When should ARBs not be used (same as ACE inhibitors)? (2)

A
  1. In patients with renal artery stenosis or AKI

2. In women who plan to become/who are pregnant, or who are breastfeeding

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69
Q

What are the possible drug interactions when using ARBs (same as ACE inhibitors)?

A
  1. Should be avoided in patient is receiving other drugs that elevate their potassium levels, there is a risk of hyperkalaemia
  2. Should be avoided in combination with NSAIDs as there is a risk of renal failure
70
Q

In which ethnicity is incidence of angioedema related to ACE inhibitor treatment, 5 times higher than other ethnicities?

A

People of African or Caribbean origin

71
Q

Name 2 nitrate drugs?

A
  1. Isosorbide mononitrate

2. Glyceryl trinitrate

72
Q

What are the 3 indicators for use of nitrates?

A
  1. Acute angina/acute coronary syndrome
  2. Prophylaxis of angina
  3. Pulmonary oedema
73
Q

Which type of nitrates: short-acting or long-acting are used in the treatment of angina/chest pain associated with acute coronary syndrome?

A

Short-acting (glyceryl trinitrate)

74
Q

Which type of nitrates are used for prophylaxis of angina, where a b-blocker and/or a calcium-channel blocker is insufficient or not tolerated?

A

Long-acting (isosorbide mononitrate)

75
Q

Nitrates are administered intravenously in the treatment of pulmonary oedema, usually in combination with which two others treatments/drugs?

A
  1. Furosemide

2. Oxygen

76
Q

What is the mechanism of actions of nitrates?

A

Nitrates are converted to Nitric oxide (NO). NO increases cyclic guanosine monophosphate (cGMP) synthesis and reduces intracellular Ca2+ in vascular smooth muscle cells, causing them to relax. This results in venous, and to a lesser extent, arterial vasodilation.

77
Q

In causing venous (and arterial) vasodilation, how do nitrates help relieve angina and cardiac failure?

A

Relaxation of the venous capacitance vessels reduces cardiac preload and left ventricular filling. These effects reduce cardiac work and myocardial oxygen demand, relieving angina.

78
Q

As well as reducing preload (this is what mostly mediates the anti-anginal effects), how do nitrates reduce afterload?

A

Nitrates relieve coronary vasospasm and dilate collateral vessels, improving coronary perfusion. They also relax the systemic arteries, reducing peripheral resistance and afterload.

79
Q

What are the side effects associated with nitrates? (3)

A

As they are vasodilators, they commonly cause:

  1. Flushing
  2. Headaches
  3. Hypotension
80
Q

What is the problem with sustained use of nitrates, particularly when taken at night when they are not so necessary?

A

Tolerance (tachyphylaxis) can be built, leading to reduce symptom relief.

81
Q

What are the contraindications for use of nitrates? (2)

A
  1. Severe aortic stenosis

2. Haemodynamic instability/hypotension

82
Q

What are nitrates contraindicated in people with severe aortic stenosis?

A

The heart is unable to increase cardiac output sufficiently through the narrowed valve area to maintain pressure in the now dilated vasculature.

83
Q

What are the possible drug interactions involved when using nitrates? (2)

A
  1. Nitrates must not be used with phosphodiesterase inhibitors (e.g. sildenafil) because these enhance and prolong the hypotensive effect of nitrates.
  2. They should be used with caution in any patient taking anti-hypertensive medication.
84
Q

Name a cardiac glycoside?

A

Digoxin

85
Q

What are the indications for use of digoxin? (2)

A
  1. Atrial fibrillation (and atrial flutter) - digoxin is used to reduce the ventricular rate, however a beta-blocker or non-dihydropyridine calcium-channel blocker is usually more effective
  2. Severe heart failure
86
Q

Digoxin is prescribed in combination with which other drugs, in the treatment of heart failure?

A

Digoxin is a third-line treatment in patients who are already taking an ACE inhibitor, beta-blocker and either an aldosterone antagonist or ARB. It is used at an earlier stage in patients with co-existing AF.

87
Q

What is the mechanism of action of digoxin?

A

Digoxin is negatively chronotropic (it reduces the heart rate) and positively inotropic (it increases the force of contraction).

88
Q

What is the mechanism of action of digoxin specifically in treating AF?

A

In the treatment of AF, digoxins therapeutic effect arises mainly via an indirect pathway involving increased vagal (parasympathetic) tone. This reduces conduction at the AV node, preventing some impulses from being transmitted to the ventricles, thereby reducing the ventricular rate.

89
Q

How is digoxin effective in treating heart failure?

A

Digoxin has a direct effect on myocytes through inhibition of Na+/K+ - ATPase pumps, causing Na+ to accumulate in the cell. As cellular extrusion of Ca2+ requires low intracellular Na+ concentrations, elevation of intracellular Na+ causes Ca2+ to accumulate in the cell, increasing contractile force.

90
Q

What side effects can digoxin cause? (6)

A
  1. Bradycardia
  2. GI disturbances
  3. Rash
  4. Dizziness
  5. Visual disturbance (blurred or yellow vision)
  6. Digoxin toxicity - as it’s therapeutic index is small - can lead to a wide range of arrhythmia’s.
91
Q

What are the contra-indications for digoxin?

A
  1. Second-degree heart block
  2. Intermittent complete heart block
  3. Ventricular arrhythmia’s
92
Q

When should the dose of digoxin be reduced?

A
  1. In patients with renal failure
  2. In patients with electrolyte imbalances: hypokalaemia, hypomagnesaemia, hypercalcaemia. (Potassium disturbance is the most important of these, as digoxin competes with potassium to bind to the Na+/K+ ATPase pump).
93
Q

How is digoxin eliminated?

A

By the kidneys

94
Q

Which drugs interact with digoxin?

A
  1. Loop and thiazide diuretics can increase the risk of digoxin toxicity by causing hypokalaemia
  2. Amiodarone, calcium-channel blockers, spironolactone and quinine, can all increase the plasma concentrations of digoxin and therefore risk of toxicity.
95
Q

Why is digoxin rarely used now?

A

Due to its narrow therapeutic window and risk of toxicity, as well as its effect relying on parasympathetic (rest and digest) tone, it tends to be lost during stress and exercise - it is still particularly an option in sedentary patients.

96
Q

Name a common anti-dysrhythmic drug?

A

Amiodarone (dronedarone, dofetilide, propafenone etc.)

97
Q

What is the indication for use of amiodarone?

A

Amiodarone is used in the management of a wide range of tachyarrhythmias, including AF, atrial flutter, SVT, ventricular tachycardia, and refractory ventricular fibrillation. It is generally used only when other therapeutic options (drugs or electrical cardioversion) are ineffective or inappropriate.

98
Q

What is the mechanism of action of amiodarone?

A
  1. Amiodarone has many effects on myocardial cells, including blockage of sodium, calcium and potassium channels, and antagonism of alpha- and beta- adrenergic receptors. These effects reduce spontaneous depolarisation (automaticity), slow conduction velocity, and increase resistance to depolarisation (refractoriness), including in the AV node. By interfering with AV node conduction, amiodarone reduces the ventricular rate in AF and atrial flutter.
  2. Amiodarone is also effective at restoring sinus rhythm.
99
Q

What are the side effects Amiodarone can cause? (7)

A 
In comparison with other antiarrhythmic drugs, amiodarone causes relatively little myocardial. depression. 
1. Hypotension
When taken chronically it can lead to:
2. Pneumonitis 
3. Bradycardia
4. AV block
5. Hepatitis 
6. Photosensitivity 
7. Thyroid abnormalities (both hypo- and hyper-).
100
Q

How long is the half-life of amiodarone?

A

On average, 58 days. It is known to have an extremely long half-life and may take months for it to be completely eliminated.

101
Q

When should use of amiodarone be avoided?

A

Avoided in patients with:

  1. Severe hypotension
  2. Heart block
  3. Active thyroid disease
102
Q

Which drugs is amiodarone known to interact with?

A

It increases plasma concentrations of digoxin, diltiazem and verapamil. This may increase the risk of bradycardia, AV block and heart failure. The doses of these drugs should be halved if amiodarone is started.

103
Q

What type of drug is clopidogrel?

A

Anti-platelet

104
Q

What are the indications for use of clopidogrel? (4)

A
  1. Acute coronary syndrome
  2. To prevent occlusion of coronary artery stents
  3. Long term secondary prevention of thrombotic arterial events in patients with cardiovascular, cerebrovascular and peripheral arterial disease
  4. To reduce the risk of intracardiac thrombus and embolic stroke in AF, where warfarin and NOACs are contraindicated
105
Q

What is the mechanism of action of clopidogrel?

A

Clopidogrel prevents platelet aggregation so that a thrombus can’t form in an atheromatous artery leading to occlusion. It also reduces the risk of arterial occlusion by binding irreversibly to adeonsine diphosphate (ADP_ receptors (P2Y12 subtype) on the surface of platelets. As this process is independent of the cyclooxygenase pathway, its actions are synergistic with those of aspirin.

106
Q

What are the possible side effects caused by clopidogrel? (3)

A
  1. Bleeding (particularly serious if GI, intracranial or following a surgery)
  2. GI upset (dyspepsia, abdo pain, diarrhoea)
  3. Thrombocytopenia (rarely)
107
Q

What are the contra-indications for use of clopidogrel? (1) and when should it be used with caution? (1)

A

Contraindication: Active bleeding - and it may need to be stopped 7 days before elective surgery
Caution: In patients with renal and hepatic impairment

108
Q

What are the possible drugs interactions when taking clopidogrel?

A

Clopidogrel is a pro-drug that requires metabolism by hepatic cytochrome P450 enzymes to its active form to have antiplatelet effect. It’s efficacy may be reduced by cytochrome P450 inhibitors (by inhibiting its activation).

109
Q

What are the examples of cytochrome P450 inhibitors?

A

Omeprazole, ciprofloxacin, erythromycin, antifungals and some SSRIs.

110
Q

Which PPIs are preferred when prescribing clopidogrel in combination with a PPI?

A

Pantoprazole or lansoprazole - as they are considered less likely to inhibit clopidogrel activation.

111
Q

What is there an increased risk of, if clopidogrel is prescribed in combination with other anti platelet/anticoagulant drugs?

A

Increased risk of bleeding

112
Q

As clopidogrel acts irreversibly, how long does it take for the effects of the drug to wear off?

A

7-10 days - the lifespan of a platelet

113
Q

What are the indications for use of aspirin? (4)

A
  1. Acute coronary syndrome and acute ischaemic stroke
  2. Long-term secondary prevention of thrombotic arterial events in patients with cardiovascular, cerebrovascular and peripheral arterial disease
  3. To reduce the risk of intracardiac thrombus and embolic stroke in AF, where warfarin and NOACs are contraindicated.
  4. To control mild-moderate pain and fever (although other drugs are usually preferred, particularly in association with inflammatory conditions).
114
Q

What are the mechanisms of action of aspirin?

A

Aspirin irreversibly inhibits cyclooxygenase (COX) to reduce production of the pro-aggregatory factor thromboxane from arachidonic acid, reducing platelet aggregate and the risk of arterial occlusion.

115
Q

What is the most common adverse effect caused by aspirin?

A

Gastrointestinal irritation

116
Q

What are the more serious side effects aspirin can cause? (2)

A
  1. GI ulceration and haemorrhage

2. Hypersensitivity reaction including bronchospasm

117
Q

What can aspirin cause when being given as a regular, high-dose therapy?

A

Tinnitus

118
Q

What are the features of an aspirin overdose?

A

They are life-threatening, including: hyperventilation, hearing changes, metabolic acidosis and confusion, followed by convulsions, cardiovascular collapse and respiratory arrest.

119
Q

What are the contraindications for use of aspirin? (3)

A
  1. Children under 16 - due to the risk of Reye’s syndrome
  2. People with aspirin hypersensitivity
  3. Third trimester of pregnancy
120
Q

When should aspirin be used with caution?

A
  1. In people with peptic ulceration (prescribe gastric protection)
  2. In people with gout (it may trigger an acute attack)
121
Q

Why in the UK is aspirin not licensed for use in primary prevention of vascular events?

A

Large scale trials have shown the potential benefits are outweighed by the increased risk of serious bleeding.

122
Q

What does rtPA stand for, and what is it?

A

Recombinant tissue plasminogen activator, it is a thrombolytic.
It is manufactured via biotechnology and is a form of a tissue plasminogen activator; a protein involved in the breakdown of blood clots. it catalyses the conversion of plasminogen to plasmin, which degrades fibrin and so breaks up thrombi.

123
Q

Name 3 rtPAs?

A
  1. Alteplase
  2. Reteplase
  3. Tenecteplase
124
Q

What are the indications for use of rtPAs?

A
  1. PE - for massive PE with haemodynamic instability
  2. MI - in acute ST elevation
  3. Ischaemic stroke - increases the chance of living independently if it is given within 4.5 hours of the onset of the stroke.
125
Q

What are the contraindications for use of rtPAs?

A
  1. Haemorrhagic stroke and head trauma
  2. Acute pancreatitis
  3. Aortic aneurysm
  4. Coma
  5. Peptic ulcer
  6. Pericarditis
  7. Oesophageal varices
  8. Bacterial endocarditis
    ….the list is endless
126
Q

When should rtPAs be used with caution?

A
  1. Elderly
  2. Hypertension
  3. When thrombolysis might give rise to embolic complications
  4. Risk of bleeding
127
Q

What are the possible side effects of using rtPAs?

A
  1. Bleeding
  2. Hypotension
  3. Allergic reactions
    4.Flushing
  4. Nausea
  5. Angina - when used for MI
  6. Cerebral oedema
  7. Back pain
  8. Convulsions
  9. Pulmonary oedema
    ….the list is endless (in BNF)
128
Q

What are the group of drugs that will have potentially serious interactions with rtPAs?

A

Any other drugs that are anti-platelet/anticoagulants/thrombolytics - all at increased risk of severe bleeding

129
Q

Which other fibrinolytic/thrombolytic drug is indicated for use in acute STEMI?

A

Streptokinase

130
Q

Name some examples of heparin and chemically-similar alternatives?

A
  1. Enoxaparin
  2. Dalteparin
  3. Fondaparinux
  4. Unfractionated heparin
131
Q

What are the indications for use of heparin(s)? (2)

A
  1. Venous thromboembolism (VTE) - including DVT and PE

2. Acute coronary syndrome

132
Q

What type of heparin is the first choice agent for venous thromboembolism, including DVT and PE?

A

Low molecular weight heparin (LMWH)

133
Q

What type of heparin or alternative is part of first-line therapy for acute coronary syndrome?

A

LMWH or fondaparinux - they improve revascularisation and prevent intracoronary thrombus progression.

134
Q

What is the mechanism of action of heparins and fondaparinux (NOACs)?

A

Thrombin and factor Xa are key components of the final common coagulation pathway that leads to formation of a fibrin clot. By inhibiting their function, heparins and fondaparinux prevent the formation and propagation of blood clots.

135
Q

What does unfractionated heparin (UFH) specifically target?

A

Unfractionated heparin activates antithrombin that, in turn, inactivates clotting factor Xa and thrombin.

136
Q

Name two examples of low molecular weight heparin, and explain how these are different to unfractionated heparin?

A

Dalteparin and enoxaparin are both examples of LMWH, and preferentially inhibit factor Xa. LWMH have a more predictable effect, so unlike UFH, do not require laboratory monitoring.

137
Q

What is fondaparinux and what does it target specifically?

A

Fondaparinux is a synthetic compound that is similar to heparin. It inhibits factor Xa only.

138
Q

Which of the heparin or alternative drugs has become the anticoagulant of choice in the treatment of ACS in the UK?

A

Fondaparinux

139
Q

What is the main adverse effect of heparins and fondaparinux?

A

Bleeding

140
Q

What is the rare, but dangerous syndrome that can be caused by heparins?

A

Heparin-induced thrombocytopenia - characterised by low platelet count and thrombosis. This immune reaction is less likely with LMWH and fondaparinux as opposed to UFH.

141
Q

When should heparins/fondaparinux be used with caution? (3)

A
  1. In patients who are at an increased risk of bleeding; including those with clotting disorders, severe uncontrolled hypertension, or recent surgery/trauma.
  2. Heparins should be avoided around the time of invasive surgery, particularly lumbar puncture and spinal anaesthesia.
  3. In patients with renal impairment
142
Q

What drug interactions are important to consider with herparins/fondaparinux?

A

When combining with other antithrombotic drugs, due to the increased risk of bleeding.

143
Q

When are both heparin and warfarin prescribed together and why?

A

Following a new diagnosis of VTE, patients will often be treated initially with both LMWH and warfarin. This is because warfarin inhibits the natural anticoagulant activity of protein C and S, and it does this before inhibiting the other clotting factors. Using LMWH provides anticoagulant cover during this initial pro-coagulant period. LMWH is stopped when the patients INR is in therapeutic range.

144
Q

What are the indications for use of warfarin?

A
  1. To prevent clot extension and recurrence in DVT and PE (venous thromboembolism)
  2. To prevent embolic complications (e.g. stroke) in AF
  3. To prevent embolic complications (e.g. stroke) in heart valve replacement.
145
Q

In terms of valve replacement, when is warfarin treatment short-term, and when is it life-long?

A

Treatment is short-term in tissue valve replacement, however it is life-long in mechanical valve replacement.

146
Q

Why is warfarin not used to prevent arterial thrombosis (e.g. MI and thrombotic stroke)

A

As this is driven by platelet aggregation, it is prevented by antiplatelet agents, such as aspirin and clopidogrel.

147
Q

What is the mechanism of action of warfarin?

A

Warfarin inhibits hepatic production of vitamin K-dependent coagulation factors and cofactors. Vitamin K must be in its reduced form for synthesis of coagulation factors. It is then oxidised during the synthetic process. An enzyme called vitamin K epoxide reductase reactivates oxidised vitamin K. Warfarin inhibits vitamin K epoxide reductase, preventing reactivation of vitamin K and coagulation factor synthesis.

148
Q

What are the side effects caused by warfarin?

A

Main adverse effect is bleeding

149
Q

What are the effects of a slight excess of warfarin?

A

Risk of bleeding from existing abnormalities such as peptic ulcers or following minor trauma

150
Q

What are the effects of a large excess of warfarin?

A

Spontaneous haemorrhage, including epistaxis or retroperitoneal haemorrhage.

151
Q

When is warfarin contraindicated? (2)

A
  1. In patients at immediate risk of haemorrhage

2. In pregnancy - specifically the first trimester, as it can cause fetal abnormalities

152
Q

When should warfarin be used with caution?

A

In patients with liver disease, who are less able to metabolise the drug, are at risk of over-anticoagulation/bleeding

153
Q

Why is the metabolism of warfarin by cytochrome P450 significant?

A

As the plasma concentration of warfarin required to prevent clotting is very close to the concentration that causes bleeding (low/narrow therapeutic index), small changes in hepatic warfarin metabolism by cytochrome P450 enzymes can cause clinically significant changes in anticoagulation.

154
Q

Name the cytochrome P450 inhibitors?

A 
SICK FACES.COM
Sodium valproate
Isoniazid 
Cimetidine 
Ketoconazole 
Fluconazole 
Alcohol..binge drinking 
Chloramphenicol 
Erythromycin (macrolides) 
Sulfonamides 
Ciprofloxacin 
Omeprazole 
Metronidazole
155
Q

What effect do cytochrome P450 inhibitors have on warfarin metabolism?

A

They decrease warfarin metabolism and increase risk of bleeding

156
Q

Name the cytochrome P450 inducers?

A 
CRAP GP'S
Carbemazepine
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbitone
Sulphonylureas
157
Q

What effect do cytochrome P450 inducers have on the metabolism of warfarin?

A

They increase warfarin metabolism and therefore increase the risk of clots.

158
Q

Why is it that many antibiotics can increase anticoagulation in patients on warfarin?

A

Antibiotics kill the gut flora which synthesise vitamin K

159
Q

Name some NOACs (novel anticoagulants)

A
  1. Rivaroxaban
  2. Apixaban
  3. Edoxaban
  4. Fondaparinux
160
Q

What is the action of NOACs?

A

They are direct factor Xa inhibitors

161
Q

What are the common side effects caused by NOACs? (4)

A
  1. GI upset - abdominal pain, constipation, diarrhoea, dyspepsia
  2. Hypotension/Dizziness
  3. Haemorrhage
  4. Nausea/Vomiting
    * BNF suggests rivaroxaban can cause these side effects more so than apixaban.
162
Q

In which patients should NOACs be avoided? (2)

A
  1. In women who are pregnant or breastfeeding

2. In patients with renal failure/liver disease

163
Q

Name 4 statins?

A
  1. Simvastatin
  2. Atorvastatin
  3. Pravastatin
  4. Rosuvastatin
164
Q

What are the indications for use of statins?

A
  1. Primary prevention of cardiovascular disease - to prevent CVD/events in people over 40, with a 10-year cardiovascular risk of >20%
  2. Secondary prevention of CVD - first-line alongside lifestyle changes, to prevent further cardiovascular events
  3. Primary hyperlipidaemia - first line, in conditions such as hypercholesterolaemia, mixed dyslipidaemia and familial hypercholesterolaemia.
165
Q

What is the mechanism of action of statins?

A

Statins reduce serum cholesterol levels. They inhibit 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase, an enzyme involved in making cholesterol. They decrease cholesterol production by the liver and increase clearance of LDL-cholesterol fro the blood, reducing LDL-cholesterol levels. They also indirectly reduce triglycerides and slightly increase LDL-cholesteorl levels. Through these effects they slow the atherosclerotic process and may even reverse it.

166
Q

What are the most common side effects that statins can cause? (2)

A
  1. Headache

2. GI disturbances

167
Q

What are the more serious side effects statins can rarely cause? (3)

A
  1. Myopathy
  2. Rhabdomyolysis
  3. Drug-induced hepatitis (due to a rise in liver enzymes ALT) - this is very rare
168
Q

What are the warnings surrounding use of statins, when should they be avoided?

A
  1. Used in caution in people with existing hepatic impairment
  2. In people with renal impairment
  3. In women who are pregnant or breastfeeding
169
Q

Through which enzyme is statin metabolised?

A

Cytochrome P450

170
Q

What are the possible drug interactions to bear in mind with statins?

A

Cytochrome P450 inhibitors will reduce the metabolism of statins, this leads to accumulation of statins in the body, which may put patients at increased risk of side effects

171
Q

What is the best course of action if a patient is prescribed a drug which is a P450 inhibitor too?

A

If they are taking the other drug on a short period only - then consider withholding the statin until that course has finished, however if it is a long-term medication, then consider reducing the dose of statin.

172
Q

Name some common cytochrome P450 inhibitors?

A 
Amiodarone 
Diltiazem/Verpamil 
Itraconazole
Macrolides
Amlodipine
Methadone
SSRIs
Omeprazole
Grapefruit juice

Drug Formulary Y3 (9 decks)

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