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Pharmacology > CV system > Flashcards

CV system Flashcards

1
Q

Name some examples of a-blockers?

A

Doxazoin, Tamsulosin, alfuzosin

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2
Q

Name some common indications for a-blockers?

A
  1. Treatment for BPH, when lifestyle changes are insufficient. 5a-reductase inhibitors may be added in selected cases.
  2. As an add-on treatment in resistant hypertension
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3
Q

How do a-blockers work?

A

a1-adrenoreceptors are found mainly in smooth muscle, including in blood vessels and the urinary tract. Stimulation induces contraction, blockade induces relaxation. a1 blockers therefore cause vasodilation and a fall in BP, and reduced resistance to bladder outflow

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4
Q

What are the important adverse effects of a-blockers?

A

They can cause postural hypotension, dizziness and syncope. This is particularly prominent after the first dose

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5
Q

When should a-blockers not be used?

A

In patients with existing postural hypotension

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6
Q

What are the important interactions of a-blockers?

A

When combined with anti-hypertensives, can result is a large BP drop

May be necessary to omit doses of anti-hypertensives on the day a-blockers are started. This is particularly the case for B blockers, which inhibit the reflex tachycardia that forms part of the compensatory response to vasodilatation

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7
Q

How are a-blockers prescribed?

A

Doxazosin is licensed both for BPH and hypertension; it is typically started at a dose of 1mg daily and increased at 1-2 week intervals according to response

Tamsulosin is licensed for BPH only. It is given at 400mcg daily

Men with BPH often have hypertension so it can be given earlier in the treatment pathway for hypertension ‘killing 2 birds with 1 stone’

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8
Q

What advice would you give to patients about taking a-blockers?

A

Advise them to start taking the medicine at bedtime to minimise the impact of dizziness

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9
Q

What is adenosine used for?

A

A first-line diagnostic and therapeutic agent in supraventricular tachycardia (SVT), usually evident on an ECG as a regular, narrow-complex tachycardia

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10
Q

How does adenosine work?

A

Increases atrioventricular node refractiveness which breaks the re-entry circuit causing SVT

“Resets heart rhythm”

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11
Q

What are important adverse effects of adenosine?

A

Bradycardia and asystole
Feels like a sinking feeling in the chest, accompanied by breathlessness and a sense of impending doom

Only lasts for a couple of seconds

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12
Q

What are the warnings for prescribing adenosine?

A

Don’t prescribe for patients with hypotension, coronary ischaemia, decompensated heart failure

It may also induce bronchospam so avoid is asthmatics and caution with COPD

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13
Q

Are there by important interactions for adenosine?

A

Dipyridamole (anti platelet agent) increases its effect so the dose should be halved

Theophylline and aminophylline reduce its effect so may need higher dose

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14
Q

How is adenosine prescribed?

A

6mg IV once only
If ineffective give 12mg dose
Needs large-bore cannula in the antecubital fossa
Give quickly then flush with 20ml of saline

Effect is evident on cardiac monitor in 10-15 seconds

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15
Q

What are the common indications of adrenaline?

A
  1. Cardiac arrest
  2. Anaphylaxis
  3. Local vasoconstriction e.g. To control mucosal bleeding in endoscopy
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16
Q

How does adrenaline work?

A

It is a potent agonist of a1,a2,B1 and B2 adrenoceptors so has have fight or flight effects

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17
Q

What are the effects of adrenaline acting on:
a1
B1
B2?

A

a1- vasoconstriction of vessels supplying skin, mucosa, and abdominal viscera
B1- increases HR, force of contraction and myocardial excitability
B2- vasodilatation of vessels supplying the heart and muscles. Also bronchodilatation and suppression of inflammatory mediator release from mast cells

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18
Q

What are important adverse effects of adrenaline?

A

Adrenaline-induced hypertension
Anxiety, tremor, headache an palpitations
Angina, MI, arrhythmias

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19
Q

Are there any warnings for use of adrenaline?

A

No CIs to use in anaphylaxis or cardiac arrest

When used to induce vasoconstriction, it should be used with caution in patients with heart disease

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20
Q

Are there any important interactions for adrenaline use?

A

B-blockers

As the a1 mediated vasoconstriction is not opposed by B2 mediated vasodilatation

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21
Q

How is adrenaline prescribed?

A

In a shockable rhythm in cardiac arrest (VF or pulseless ventricular tachycardia) , adrenaline is given 1mg IV after the 3rd shock and repeated every 3-5 mins

In a non-shockable rhythm, adrenaline 1mg IV is given instantly, and repeated every 3-5 mins

In anaphylaxis, give 500mcg IM and repeat after 5 mins if necessary

Can be mixed with LA if being used sub-cut to induce local vasoconstriction

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22
Q

What are some examples of aldosterone antagonists?

A

Spironolactone, eplerenone

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23
Q

What are the common indications for aldosterone antagonists?

A
  1. Ascites and oedema due to liver cirrhosis- spironolactone is 1st line diuretic
  2. Chronic heart failure- moderate severity, usually as an addition to BB, ACEi/ARB
  3. Primary hyperaldosteronism- for patients awaiting surgery or for whom surgery is not an option
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24
Q

How do aldosterone antagonists work?

A

They inhibit the effect of aldosterone by competitively binding to the aldosterone receptor- increasing sodium and water excretion and potassium retention

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25
Q

What are important adverse effects of aldosterone antagonists?

A

Hyperkalaemia- which can lead to muscle weakness, arrhythmias and cardiac arrest

Gynaecomastia from spironolactone

Liver impairment and jaundice which can cause Stevens-Johnson syndrome

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26
Q

Which patients are aldosterone antagonists contraindicated or warned in?

A

Those with severe renal impairment, hyperkalaemia and Addison’s disease

They can also cross the placenta during pregnancy so should be avoided in pregnant and lactating women

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27
Q

Are there any drugs that interact with aldosterone antagonists?

A

Those that elevate potassium- ACEi, ARBs

Could be beneficial in heart failure though

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28
Q

How are aldosterone antagonists prescribed?

A

Orally, should be taken with food

Usually a single daily dose, e.g. Spironolactone 100mg daily for ascites compared to 25mg daily for heart failure

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29
Q

How should be aldosterone antagonists be monitored?

A

Renal function and serum potassium

Monitor efficacy through clinical improvement e.g reduction of ascites

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30
Q

What is amiodarone used for?

A

Used in tachyarrhythmias (AF, atrial flutter, SVT, VT and VF)
It is used when other drugs haven’t worked

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31
Q

How does amiodarone work?

A

Blockades sodium, potassium and calcium channels, and antagonises a- and B-adrenergic receptors

These reduce spontaneous conduction, slow conduction velocity and increase resistance to depolarisation (refractoriness)

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32
Q

What are the adverse effects of amiodarone?

A

Causes relatively little myocardial depression

Can cause hypotension

When taken chronically it can cause pneumonitis, bradycardia, hepatitis, thyroid abnormalities (due to iodine content), photosensitivity and grey discolouration

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33
Q

What are the warnings surrounding amiodarone?

A

Should be avoided in patients with severe hypotension, heart block and active thyroid disease

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34
Q

What are the important interactions with amiodarone?

A

Reacts with many- notably digoxin, diltiazem and verapamil which can increase risk of bradycardia and AV block

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35
Q

How is amiodarone prescribed?

A

In cardiac arrest, it is given for VF or pulseless VT, 300mg IV, followed by 20ml of 0.9% saline or 5% glucose as a flush

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36
Q

How is amiodarone administered?

A

Given as a bolus injection in cardiac arrest
Outside ca, should be given via a central line if repeat infusions are administered

Should be continuous cardiac monitoring

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37
Q

Name some examples of angiotensin receptor blockers?

A

Losartan, candasartan, irbesartan

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38
Q

What are ARBs indicated for?

A

Generally used when ACEis are not tolerated due to cough

  1. Hypertension
  2. Chronic heart failure
  3. Ischaemic Heart Disease
  4. Diabetic nephropathy and CKD with proteinuria
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39
Q

How do ARBs work?

A

They block the action of angiotensin II on the angiotensin type 1 (AT) receptor

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40
Q

What are the adverse effects of ARBs?

A

They can cause hypotension, hyperkalaemia and renal failure

They don’t cause a cough as they don’t affect the bradykinin mechanism

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41
Q

Which patients are ARBs warned in?

A

Should be avoided in patients with renal artery stenosis or AKI, and cautioned in women who could be pregnant and those who are breastfeeding

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42
Q

What are the important interactions of ARBs?

A

Avoid potassium elevating drugs- K-sparing diuretics, potassium supplements

The combination of NSAIDs with ARBs increases the risk of nephrotoxicity

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43
Q

How are ARBs prescribed?

A

Orally
E.g losartan 12.5mg daily in HF or 50mg daily in other indications

Start low and titrate up

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44
Q

How are ARBs taken?

A

Can be taken with or without food, it is best to take the first dose before bed to avoid reduce symptomatic hypotension

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45
Q

What tests need to be done before and during ARB treatment?

A

U&Es, renal function before and 1-2 weeks into treatment and after increasing the dose

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46
Q

When should ARBs be stopped?

A

When serum creatinine rises more than 30% or the eGFR falls more that 25%

If serum potassium goes above 5, firstly stop nephrotoxic drugs and if it continues to be high, reduce the dose of the ARB

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47
Q

What are examples of ACE inhibitors?

A

Ramipril, lisinopril, perindopril

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48
Q

What are the clinical indications for ACE inhibitors?

A
  1. Hypertension
  2. Chronic heart failure
  3. Ischaemic heart disease
  4. Diabetic nephropathy and CKD
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49
Q

How do ACE inhibitors work?

A

Prevent the conversion of angiotensin I to II.

In turn it lowers BP, slows progression of CKD and reduces venous return (has benefits in HF)

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50
Q

What are the important adverse effects of ACEi?`

A

Hypotension, persistent dry cough and hyperkalaemia
They can cause or worsen renal failure

Rare side effects include angioedema and anaphylactoid reactions

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51
Q

What are the warnings for taking ACEi?

A

Should be avoided in patients with renal artery stenosis or AKI, in women who could be pregnant or are breastfeeding

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52
Q

What are the important interactions for ACE inhibitors?

A

Avoid potassium-elevating drugs including potassium sparing diuretics and K supplements

The combination of an NSAID and ACEi increases the dose of nephrotoxicity

53
Q

How are ACE inhibitors prescribed?

A

Orally
A common choice is Ramipril 1.25mg daily in heart failure or nephropathy, or 2.5mg daily in most other indications
This is titrated up to a max of 10mg daily over a period of weeks

54
Q

How are ACE inhibitors taken?

A

With or without food

It is best to take the first dose before bed to reduce symptomatic hypotension

55
Q

How are ACE inhibitors monitored?

A

Monitor efficacy clinically
For safety, check U&Es and renal function before starting treatment. Repeat these 1-2 weeks into treatment and after increasing the dose

56
Q

When should ACE inhibitors be stopped/ changed?

A

Stop ACEi if the serum creatinine conc rises more than 30% or the eGFR falls more than 25%

If serum potassium rises above 5, stop any nephrotoxic drugs. If it continues to remain high, reduce the dose of the ACEi

57
Q

Name some examples of antimuscarinics used for CV and GI causes?

A

Atropine, hycosine bromide, glycopyrronium

58
Q

What are the indications for antimuscarinics for CV and GI causes?

A
  1. Atropine is used as a first-line treatment in the management of severe or symptomatic bradycardia to increase heart rate
  2. Treatment for IBS (particularly hycosine bromide) due to their anti-spasmodic effect
  3. Reducing copious respiratory secretions in the dying patient (hycosine bromide)
59
Q

How do antimuscarinics work?

A

The are a competitive inhibitor of acetylcholine at the muscarinic receptor
As a result, they increase HR and conduction, reduce smooth muscle tone and peristaltic contraction, including the gut and urinary tract, and reduce secretions from glands in the resp tract and gut
In the eye they cause relaxation of the pupillary constrictor and ciliary muscles

60
Q

What are the important adverse effects of antimuscarinics?

A

Tachycardia, dry mouth, constipation, urinary retention (in patients with BPH), blurred vision
‘Can’t see, can’t wee, can’t shit, can’t spit’

Some antimuscarinics have central effects, which may precipitate drowsiness and confusion, particularly in the elderly

61
Q

What are the warnings for taking anti-muscarinics?

A

Should be used in caution in patients susceptible to acute-closure glaucoma, in whom they can precipitate a dangerous rise in intraocular pressure

Cautioned in patients with increased risk of arrhythmias

62
Q

What are the important interactions with antimuscarinics?

A

Others with anti-muscarinic effects, such as tricyclic antidepressants

63
Q

How are anti-muscarinics prescribed?

A

For bradycardia, atropine is usually preferred and given IV with incremental doses (e.g. 500mcg every 1-2 mins) until an acceptable HR is reached (some practitioners recommend no less than 600mcg as any less can SLOW the HR)

For IBS, taken orally e.g HB (Buscopan) 10MG 8-hourly- available w/o a prescription

For resp secretions, hycosine butylbromide or hycosine hydrobromide is given subcut

64
Q

Name some examples of anti-platelets/ ADP-receptor antagonists?

A

Clopidogrel, icagrelor, prasugrel

65
Q

What are anti-platelets indicated for?

MORE CARDS + ASPIRIN CARDSN IN BLOODS DECK

A
  1. Treatment of ACS (with aspirin)
  2. To precvent occlusion of coronary artery stents (with aspirin)
  3. Long term CV secondary prevention of thrombotic arterial events
66
Q

Name some examples of B-blockers?

A

Bisoprolol, atenolol, propranolol, metoprolol, carvedilol

67
Q

What are B-blockers used for?

A
  1. Ischaemic heart disease- improve symptoms and prognosis associated with angina and ACS
  2. Chronic heart failure
  3. AF- reduce ventricular rate and maintain sinus rhythm
  4. SVT- to restore sinus rhythm
  5. Hypertension- may be used with other therapies are insufficient or inappropriate
68
Q

How do B blockers work?

A

They reduce the force of contraction and speed of conduction in the heart

They also prolong the refractory period of the AV node to slow the ventricular rate in AF

They also reduce BP by reducing renin secretion in the kidney

69
Q

What are the adverse effects of B-blockers?

A

They commonly cause fatigue, cold extremities, headaches and GI disturbances e.g. nausea
They can cause sleep disturbances and nightmares
They may cause impotence in men

70
Q

What are the warnings surrounding B-blockers?

A

Avoid in patients with asthma as they can cause bronchospasm
They should be avoided in patients who are haemodynamically unstable and are contraindicated in heart block
B blockers generally require dose reduction in hepatic failure

71
Q

How are beta blockers prescribed?

A

Orally
Dose varies according to indication
When starting, you should chose a drug with a short half-life so it will be more responsive to dose adjustments quicker
e.g. Metoprolol 12.5mg 8-hourly initially, later increased to 25mg 8-hourly
Should be taken at roughly the same time each day

72
Q

Name some examples of calcium channel blockers?

A

amlodipine, nifedipine, diltiazem, verapamil

73
Q

Name some common indications for CCBs?

A
  1. Amlodipine and nifedipine are used for the 1st and 2nd line treatment of hypertension, to reduce the risk of stroke and MI
  2. Control stable angina
  3. Diltiazem and verapamil are used to control cardiac rate in people with SVT, atrial flutter and AF
74
Q

How do CCBs work?

A

They decrease calcium ion entry into vascular and cardiac cells, reducing intracellular calcium conc. This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure

In the heart, the reduce myocardial contractility. They suppress cardiac conduction, particularly across the AV node, slowing ventricular rate and myocardial O2 demand- preventing angina

75
Q

What are the different classes of CCBs?

A

Dihydropyridines- amlodipine and nifedipine, relatively selective for vasculature
Non-dihydropyridines- more selective for the heart, verapamil being the most cardioselective. Diltiazem also has some effect on blood vessels

76
Q

What are the important adverse effects of CCBs?`

A

Amlodipine and nifedipine- ankle swelling, flushing, headache, palpitations

Verapamil- most commonly causes constipation, and less commonly bradycardia, heart block and cardiac failure

Diltiazem- can cause any of the above SEs

77
Q

What are the warnings surrounding CCBs?

A

Verapamil and diltiazem should be used in caution in patients with poor left ventricular function as they can precipitate or worsen heart failure. Should be avoided in people with AV nodal conduction delay

Amlodipine and nifedipine should be avoided in patients with unstable angina as vasodilation causes a reflex increase in contractility and tachycardia, which increases myocardial O2 demand

In patients with severe aortic stenosis, amlodipine and nifedipine should be avoided as they can provoke collapse

78
Q

What do CCBs interact with?

A

Non-dihydropyridine CCBs should not be prescribed with beta-blockers except under close supervision, as they are both negatively inotropic and can cause HF, bradycardia and even asystole

79
Q

How are CCBs prescribed?

A

Usually taken orally
Amlodipine has a plasma half-life of 35-50 hours and is suitable for once-daily administration
By contrast, nifedipine has a half-life of 2-3 hours, verapamil (2-8 hours) and diltiazem (6-8 hours)

Diltiazem and nifedipine are available as SR 8-hourly, and MR taken 12-hourly

Example regimens:
Hypertension- amlodipine 5-10mg OD
Angina- diltiazem MR 90mg orally 12-hourly
Supraventricular arrhythmias- verapamil 40-120mg 8-hourly

80
Q

How are CCBs monitored?

A

BP monitoring for hypertension
Enquire about chest pain for angina
Pulse rate from examination or ECG

81
Q

What is digoxin used for?

A
  1. In AF and atrial flutter, it is used to reduce the ventricular rate. However a BB or CCB is usually more effective
  2. In severe heart failure, it is an option in patients who are already on an ACEi
82
Q

How does digoxin work?

A

It is negatively chonotropic (reduces the heart rate) and positively inotropic (increases force of contraction)

In AF it increases vagal tone (parasympathetic) which reduces contraction at the AV node. However this can be lost in stress and failure exercise, so it is rarely used on its own

In heart failure, it increases contractile force by directly affecting the myocytes, causing Ca to accumulate in the cell

83
Q

What are the important adverse effects of digoxin?

A

Bradycardia, GI disturbance, rash, dizziness, visual disturbance (blurred or yellow vision)
It has a narrow therapeutic index meaning the toxic dose is close to the therapeutic dose. Toxicity can cause a wide range of arrhyhmias

84
Q

What are the warnings for taking digoxin?

A

It can worsen conduction abnormalities, so is contraindicated in second-degree heart block and intermittent complete heart block

It should not be used in patients with or at risk of ventricular arrhythmias

The dose should be reduced in renal failure, as digoxin is eliminated by the kidneys

Certain electrolyte abnormalities can increase the risk of digoxin toxicity, such as hypokalaemia, hypomagnesaemia and hypercalaemia

85
Q

What are the important interactions of digoxin?

A

Loop and thiazides diuretics can increase the risk of digoxin toxicity by causing hypokalaemia

Amiodarone, CCBs, spironolactone and quinine can all increase plasma conc of digoxin and therefore increase toxicity

86
Q

How is digoxin prescribed?

A

Available as an oral or IV preparation
The effect of IV digoxin is 30 mins, whereas 2 hours following oral

A loading dose is required for rapid effect- 500mcg of digoxin followed by 200-500mcg 6 hours later, depending on response
There after, the usual maintenance dose is 125-250mcg daily

87
Q

What does an ECG show for a therapeutic dose?

A

ST-segment depression (the reverse tick sign)

88
Q

Name some examples of loop diuretics

A

Furosemide, bumetanide

89
Q

What are the indications for loop diuretics?

A
  1. For relief of breathlessness in acute pulmonary oedema in conjunction with oxygen and nitrates
  2. For symptomatic treatment of fluid overload in chronic heart failure
  3. For symptomatic treatment of fluid overload in other oedematous states e.g. Due to renal disease or liver failure
90
Q

How do loop diuretics work?

A

They act of the ascending limb of the loop of Henle, where they inhibit the Na+/K+/2Cl- co-transporter

This prevents these ions leaving the lumen for the epithelial cells, so has a diuretic effect

In addition, they also have a direct effect on blood vessels, causing dilatation of capacitance veins. In acute heart failure, this reduces preload and improve some contractile function of the ‘overstretched’ heart muscle

91
Q

What are the important adverse effects of loop diuretics?

A

Dehydration and hypotension
You can associate loop diuretics with almost any low electrolyte state

At high doses, loop diuretics can also lead to tinnitus and hearing loss

92
Q

What are the warnings for loop diuretics?

A

They are contraindicated in patients with severe hypovolaemia or dehydration

They should be used with caution in patients at risk of hepatic encephalopathy (where hypokalaemia can cause or worsen coma) and in pts with severe hypokalaemia or hyponatraemia

Taken chronically, they can worsen gout

93
Q

What are the importantly interactions for loop diuretics?

A

They have the potential to affect drugs that are excreted by the kidneys e.g. Lithium levels are increased due to reduced excretion
Increased risk of digoxin toxicity due to diuretic-associated hypokalaemia

They can increase the ototoxicity and neohrotoxiciyy of aminoglycosides

94
Q

How are loop diuretics prescribed?

A

They are available in oral and IV preparations

In the management of acute pulmonary oedema, you usually prescribe the initial dose of the loop diuretic IV, due to its more rapid and reliable effect. A typical dose is furosemide 40mg IV

Then may need additional bonuses or regular oral medication

95
Q

When should oral maintenance doses of loop diuretics be prescribed?

A

Taken in the morning, with 2nd dose in early afternoon, to avoid nocturia

96
Q

How are loop diuretics monitored?

A

Improvement in symptoms, tachycardia, hypertension and oxygen requirement

In longer term therapy, monitor symptoms, signs and body weight

For safety, regularly monitor serum sodium, potassium and renal function particularly in the 1st few weeks

97
Q

Name some examples of thiazide and thiazide-like diuretics?

A

Bendroflumethazide, indapamide, chlortalidone

98
Q

What are thiazides diuretics used for?

A
  1. As an alternative treatment for hypertension where a CCB would otherwise be used; bunks unsuitable due to oedema or there are features heart failure
  2. Add-on treatment for hypertension in patients whose BP is not adequately controlled by a CCB plus a ACEi/ARB
99
Q

How do thiazide diuretics work?

A

They inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron. This prevents reabsorption of sodium and its osmotically associated water. This resulting diuresis causes an initial fall in extracellular fluid volume. Over time, compensatory change from the RAS tends to reverse this. The longer-term anti hypertensive effect may be mediated by vasodilatation

100
Q

What are the important adverse effects of thiazide diuretics?

A
  • Preventing sodium reabsorption from the nephron can cause hyponatraemia
  • This can also lead to hypokalaemia, which in turn can lead to cardiac arrhythmias
  • Can also cause impotence in men
101
Q

What are the warnings surrounding thiazide diuretics?

A

They should be avoided in patients with hypokalaemia and hyponatraemia. As they reduce uric acid excretion, they may precipitate acute attacks in patients with gout

102
Q

What are the important interactions with thiazide diuretics?

A

They effectiveness may be reduced by NSAIDs (not aspirin though)
Should not be combined with other potassium lowering drugs such as loop diuretics

103
Q

Why is combining ACEi/ARBs and thiazide diuretics useful?

A

Thiazides cause hypokalaemia
ACEi/ARBs cause hyperkalaemia
They also have a synergistic BP lowering effect, therefore combination is useful for BP control and maintaining potassium balance

104
Q

How are thiazides prescribed?

A

Orally, best taken in the morning so it doesn’t wake them up at night needing a wee
Indapamide (e.g. 2.5mg daily) and chlortalidone (12.5-25mg daily) are recommended for hypertension

105
Q

What should be monitored during prescription of thiazide diuretics?

A

Measure patients BP and severity of oedema
Measure the patient’s serum electrolyte concentrations before starting the drug, at 2-4 weeks into therapy, and after any change in therapy that might alter electrolyte balance

106
Q

What is lidocaine indicated for?

A
  1. Local anaesthetic e.g. urinary catheterisation and minor procedures e.g. suturing
  2. Uncommonly as an anti-arrhythmic drug in VT and VF refractory to electrical cardioversion
107
Q

How does lidocaine work?

A

Blocks voltage-gated sodium channels on the surface membrane

In the heart, it reduces the action potential, slows conduction velocity and increases the refractory period. These effects may terminate VT and improve the chances of successfully treating VF

108
Q

What are the important adverse effects of lidocaine?

A

Initial stinging sensation
Also drowsiness, restlessness, tremor and fits in systemic administration
In overdose it can cause hypotension and arrhythmias

109
Q

What are the warnings with lidocaine?

A

It depends heavily in hepatic blood from for its elimination therefore a lower dose should be used in states of reduced cardiac output

110
Q

What are the important interactions with lidocaine?

A

As the duration of action of LA depends on how long they stay in contact with the neurons, co-administration produces a desirable interaction that may prolong the LA effect

111
Q

How is lidocaine prescribed?

A

For urinary catheterisation, it is a gel with an antiseptic agent- called Instillagel (dose is 6-11mL in the once-only section)

For minor procedures, usually use a 1% (10mg/mL) solution of lidocaine hydrochloride. The max dose is 200mg or 3mg/kg, whichever is lower (7mg/kg or up to 500mg is permitted with it is combined with adrenaline)

112
Q

Name some examples of nitrates?

A

Isosorbide mononitrate, glyceryl trinitrate

113
Q

What are nitrates used for?

A
  1. Short-acting nitrates e.g. glyceryl trinitrate are used in the treatment of acute angina and chest pain associated with acute coronary syndrome (ACS)
  2. Long-acting nitrates e.g. isosorbide mononitrate are used for the prophylaxis of angina where a B-blocker and/or a calcium channel bocker are insufficient or not tolerated
  3. IV nitrates are sued in the treatment of pulmonary oedema, usually in combination with furosemide and oxygen
114
Q

How do nitrates work?

A

Nitrates are converted into (NO. NO increases cyclic guanosine monophospate (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 vasodilatation.
Relaxation of the venous capacitance vessels reduces cardiac preload and left ventricular filling. These effects reduce cardiac work and myocardial oxygen demand, relieving angina and cardiac failure

Nitrates can relieve coronary vasospasm and dilate collateral vessels, improving coronary perfusion

115
Q

What are the important adverse effects of nitrates?

A

As vasodilators, nitrates commonly cause flushing, headaches, light-headedness and hypotension.

Sustained use of nitrates can lead to tolerance, with reduced symptom relief despite continued use. To prevent this, time doses to ensure that there is a ‘nitrate-free period’ every day during a time of inactivity, usually overnight. E.g take doses morning and early afternoon rather than morning and night

116
Q

What are the warnings surrounding nitrates?

A

They are contraindicated in patients with severe aortic stenosis, in whom they may cause cardiovascular collapse
Nitrates should also be avoided in patients with haemodynamic instability, particularly hypotension

117
Q

What are the important interactions with nitrates?

A

They must NOT be used with phosphodiesterase (PDE) inhibitors (e.g. sildenafil) because these enhance and prolong the hypotensive effects of nitrates
They should also be used in caution in patients take antihypertensive medication

118
Q

How are nitrates prescribed?

A

GTN is taken sublingually as tablets or spray for immediate relief of chest pain

In patients with ACS or heart failure, it is prescribed as a continuous IV infusion. ISMN has a plasma half-life of 4-5 hours and is prescribed 2-3 times a day as immediate-release tablets for the prevention of current angina. ISMN is also available as MR tablets or transdermal patches, which are prescribed once-daily

119
Q

How is GTN administered?

A

Usually administered as 50mg in 50mL (1mg/mL). Give nursing staff clear instructions on the starting dose e.g 1ml/hr. You should provide instructions on how to increase the dose to relieve symptoms e.g. increase rate by 0.5mg/hour every 15-20 mins until chest pain is relieved while avoiding hypotension (systolic BP >90mmHg)

120
Q

What should be monitored during nitrate prescription?

A

The best indicator of efficacy are the patients symptoms. When administering nitrates by IV infusion, blood pressure should be monitored frequently, and the infusion rate adjusted to ensure the systolic BP does not drop below 90mmHg

121
Q

Name some examples of strong opioids

A

Morphine, oxycodone

122
Q

What are strong opioids prescribed for?

A
  1. Rapid relief of acute severe pain, including post-operative pain and pain associated with acute MI
  2. Relief of chronic pain, when paracetamol, NSAIDs and weak/moderate opioids are insufficient
  3. Relief of breathlessness in the context of end-of-life care
  4. Relief
123
Q

How do strong opioids work?

A

Opiates- morphine
Synthetic analogues- oxycodone
They work by activating opioid u-receptors in the CNS. They reduce neuronal excitability and pain transmission, therefore reducing sympathetic nervous system- which can also reduce cardiac work and oxygen demand in acute MI and pulmonary oedema

124
Q

What are the important adverse effects of strong opioids?

A
  • They cause respiratory depression by reducing respiratory drive. This may cause euphoria and detachment, and in higher doses, neurological depression
  • Can cause N&V at the beginning of use
  • Pupillary constriction can occur
  • Constipation due to increased smooth muscle tone and reduced motility
  • Tolerance and dependence over time, withdrawal reaction
125
Q

What are the warnings surrounding opioids?

A

Doses should be reduced in hepatic failure and renal impairment and in the elderly
Don’t give opioids in resp failure except under senior guidance e.g. palliative care
Avoid opioids in biliary colic, as they may cause spasm of the sphinctor of Oddi, which may worsen pain

126
Q

What are the important interactions for strong opioids?

A

They should ideally not be used with other sedating drugs e.g. antipsychotics, benzodiazepines, TCAs

127
Q

How are strong opioids prescribed?

A

Acute severe pain- IV morphine 2-10mg

Chronic pain- oral route. Immediate release oral morphine is preferred initially (e.g. Oramorph 5mg every 4 hours). Then, having found the optimum dose, this is converted to a MR form (e.g. MST Continus 15mg every 12 hours). Alongside regular treatment, ‘breakthrough analgesia’ should be prescribed. Prescribe Oramorph IM about 1/6th of the total daily regular dose (e.g. 5mg 2-hourly) in the as-required section

128
Q

What can be given for the nausea and constipation experienced with opioid prescription?

A

Metocloproamide for nausea

Senna for constipation

129
Q

What are the clinical features of opioid withdrawal?

A

Anxiety, pain, breathlessness, pupil dilatation, cool and dry skin (hence the phrase ‘cold turkey’)

Pharmacology (9 decks)

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