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Chapter 4 Local anaesthetics and analgesics

drugs that are classed as analgesic mixtures. For

example, co-codamol tablets contain paracetamol

and codeine phosphate in varying ratios (available

preparations are codeine 8mg/paracetamol 500mg,

codeine 15mg/paracetamol 500mg and codeine

30mg/paracetamol 500mg). Another analgesic

mixture that you will come across regularly is

co-dydramol, which contains dihydrocodeine 10mg

and paracetamol 500mg per tablet.

Tramadol

Tramadol is a strong analgesic painkiller but a

moderate strength opioid. It can be used in acute

and chronic pain. Like other opioids, it has the

potential to become addictive and patients should

be monitored for signs of this as well as tolerance

(the need for more of the drug to produce the same

response), and the lowest possible does to produce

the analgesic effect should be administered. Daily

does of over 400mg should not be given. Although

able to be used in chronic pain, the manufacturer

recommends that tramadol should not be adminis-

tered for longer than absolutely necessary. Dose

adjustments (reductions) may be needed in the

over-75s and its use is not recommended in chil-

dren under 12.

When a patient starts taking any opioid, it is very

important that you warn them of the possible sed-

ative effects and discuss the dangers of driving or

operating heavy machinery. This is a requirement

of legislation amending the Road Traffic Act to

incorporate The Drug Driving (Specified Limits)

(England & Wales) (Amendment) Regulations 2015.

Opioid antagonists

As discussed above, respiratory depression is a

side-effect of opiates. Therefore, in opioid over-

dose, an antidote is necessary. This comes in the

form of a drug called naloxone, which attracts

strongly to all three opioid receptors. Naloxone

blocks the actions of morphine and our own endor-

phins by occupying the opioid receptors without

bringing about any response, so effectively stop-

ping anything else connecting to the receptor.

Naloxone therefore quickly reverses the effects of

opioid drugs.

Drugs for neuropathic pain

Neuropathic pain is caused by damage to nerves

and often does not respond to the common pain-

killers we have discussed so far. Newer drugs, or

drugs used for other purposes have been found to

be beneficial in managing this type of pain in some

patients. Very often these drugs are prescribed to

patients with long-term intractable pain who may

be under the management of a specialist pain team

or in a shared care arrangement between the pain

team and their GP.

Amitriptyline

Amitriptyline is a tricyclic antidepressant drug that

has been used for many years. As other antidepres-

sants were developed this drug, due to its many

side-effects, became less favoured in the treatment

of depression (see Chapter 12 for its mechanism of

action), although evidence is emerging of its use-

fulness in treating pain that has a neuropathic com-

ponent. The BNF section on managing neuropathic

pain suggests its use, or its close relative nortrip-

tyline, or the use of anti-epileptic medicines. The

use of amitriptyline in this condition is unlicensed

but there is a growing body of evidence to sup-

port its use as seen in a Cochrane review of 2015

(Moore et al. 2015).

Gabapentin and pregabalin

These two drugs are anti-epileptic medications

and are sometimes referred to as gabapentinoids.

Clinical tip

The main clinical use of naloxone is

to treat respiratory depression caused by

opioid drugs in overdose, whether acciden-

tal or intentional. It is usually given intra-

venously, and its effects are immediate.

It has a relatively short half-life, as it is

quickly metabolized by the liver. Therefore,

when treating a patient, you may see the

drug repeatedly used in order to maintain

respiratory function.

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Chapter 4 Local anaesthetics and analgesics

The pharmacodynamic mechanism is to block

calcium channel mediated neurotransmission but

the actual link to the analgesic effect is poorly

understood and may be related to activity in the

dorsal horn of the spinothalamic tract (Chinchol-

kar 2018). These drugs have been licensed for

treatment of peripheral neuropathic pain and their

use has increased dramatically over recent years

(Morrison et al. 2017). They are of proven benefit

to some patients – many patients and prescribers

find the side-effects and risk of adverse reactions

to outweigh the potential benefits. There is a risk

of addiction and concomitant misuse with opioid

medication and as such they became controlled

drugs, subject to the Misuse of Drugs Act 1971 in

2019.

Case studies

Dawn Mason, a 40-year-old woman, has undergone major abdominal surgery. The medi-

cal staff have decided to change her analgesia from opioids to NSAID medication as she is

4 days post-surgery. A health care assistant approaches you and asks you to explain the mode

of action of the different types of analgesia and why the patient is now stepping down from one

set of analgesia to another. Discuss this with reference to:

■ the mode of action of these two drugs;

■ the importance of stepping down post-operative analgesia;

■ the maintenance required to achieve a steady plasma concentration of analgesic;

■ how you would put this information into terms that the health care assistant will understand.

Alex Smith is a 9-year-old boy who has sustained a broken arm after falling from his bike. The

doctor has prescribed him paracetamol and ibuprofen. The dose he can have for each drug is:

■ ibuprofen 200mg every 6–8 hours;

■ paracetamol 500mg every 4–6 hours, maximum 2g in 24 hours.

You must explain to Alex and his parents how these drugs work and the importance of regular

medication to manage Alex’s pain. Discuss this with reference to:

■ pharmacodynamics: mode of action of the two drugs;

■ pharmacokinetics: the need for regular dosing to achieve a therapeutic plasma concentration;

■ how you would put this information in terms that Alex and his parents will understand.

Michael Nozic is a 56-year-old male who has a history of osteoarthritis, worsened by hip dys-

plasia. His pain has become much less tolerable during the past year and his ability to carry

out certain activities of living has been reduced drastically. He was admitted for a total hip re-

placement and has just returned from theatre to your ward. He has had a spinal anaesthetic and

sedation during the procedure.

With reference to his spinal anaesthetic, what nursing observations would you make on Mr

Nozic during his immediate post-operative care?

Ruby Mtumba is a 71-year-old female. She has been referred to the pain team because her

pain is becoming more persistent and widespread. She is complaining of pain in her lower back,

neck and shoulders. This lady is a widow, but her daughter has moved in to help her, especially

as the pain is stopping her carry out daily activities.

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Chapter 4 Local anaesthetics and analgesics

With reference to the WHO’s analgesic ladder (see Figure 4.8), explain how this lady’s pain

should have been pharmacologically managed.

Jonti Williams is aged 35 and has neuropathic pain resulting from a slipped disc causing sciatica.

Jonti has Down’s Syndrome and suffers from focal epileptic seizures. His current anti-epileptic

medication is gabapentin 300mg three times daily.

Using the BNF, look at the range of medication that may be prescribed for Jonti’s pain, and any

potential interactions with his current medication.

→

Key learning points

Introduction

▶

Pain alerts us to tissue damage.

▶

Pain is a defence mechanism.

▶

We can suffer pain without tissue damage.

▶

Pain is a difficult concept to define.

▶

At rest, the inside of a neurone carries a negative charge.

▶

For the neurone to fire, the inside must become positive.

▶

Sodium moves into the neurone to allow it to become positively charged.

▶

The pre-synaptic neurone allows calcium to enter.

▶

The neurotransmitter allows the post-synaptic neurone to be excited or inhibited.

▶

Pain is received by nociceptors.

▶

Nociceptors are fired by heat, pressure or chemicals.

▶

Nociceptors are non-adapting, high-threshold fibres.

▶

Pain is transmitted by A-delta and C fibres.

▶

A-delta and C fibres synapse in the dorsal horn of the spinal cord.

▶

The pain impulse is interpreted in several areas in the brain.

▶

The analgesic system is a descending one.

▶

It is thought to close the gate to pain stimuli.

▶

Endorphins, dynorphins and enkephalins are important in modifying pain.

▶

Nociceptive pain results from tissue damage.

▶

Neuropathic pain is damage to nerves in the peripheral or central nervous system.

▶

The duration of pain results in it being classified as either acute or chronic.

Local anaesthetics

▶

Produce a reversible loss of sensation.

▶

There are two classes: esters and amides.

▶

Block sodium channels in the neurone.

▶

Usually used as dilute preparations (e.g. lidocaine 1%).

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Chapter 4 Local anaesthetics and analgesics

▶

Can cause vasodilation (so are often given with adrenaline).

▶

Can be given topically, via infiltration, as a nerve block, as an epidural, as a spinal anaesthet-

ic or as an intravenous injection.

▶

Can cause central nervous and cardiovascular side-effects.

Non-steroidal anti-inflammatory drugs

▶

Used for mild-to-moderate pain.

▶

Lower body temperature and have anti-inflammatory properties.

▶

Block the production of prostaglandins.

▶

Block cyclooxygenase pathways.

▶

Limit prostaglandin effects on the nociceptors.

▶

Have marked gastrointestinal and renal side-effects.

▶

Paracetamol damages the liver if the recommended dose is not followed.

▶

Paracetamol overdose is treated with N-acetylcysteine.

Opioid analgesics

▶

Given for moderate-to-severe pain.

▶

Work on receptors in the central nervous system.

▶

Some drugs are natural compounds, while some are synthetic agents.

▶

Block entry of calcium into pre-synaptic neurone.

▶

Open potassium channels making it harder for the pain neurone to fire.

▶

Main effects are on the central nervous system and gastrointestinal tract.

▶

Morphine is the gold standard by which other opioids are measured.

▶

Morphine can cause tolerance and dependence.

▶

Fentanyl is a powerful synthetic opiate analgesic similar to, but approximately 100 times more

potent than, morphine.

▶

Fentanyl is used to treat patients with severe pain, or to manage pain after surgery.

▶

Fentanyl is also used to treat people with chronic pain who are physically tolerant to opiates.

▶

Codeine is a weak opioid.

▶

Tramadol is an opioid of moderate strength.

▶

Naloxone is given to reverse the effects of morphine.

Drugs for neuropathic pain

▶

Amitriptyline is a tricyclic antidepressant useful in managing neuropathic pain.

▶

Gabapentin and pregabalin are anti-epileptic drugs useful in managing neuropathic pain.

They are controlled drugs.

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Chapter 4 Local anaesthetics and analgesics

Calculations

1 Pethidine 100mg in 2mL is available to you. However, the patient has been prescribed

75mg. How much do you give?

2 A patient requires 1000mg of paracetamol in liquid form. The stock you have contains 125mg

in 5mL. How many mL would you give?

3 Codeine is available in three strengths as tablets: 5mg, 10mg and 20mg. What is the least

number of tablets you can give if the prescription is a dose of 50mg?

4 900mg of gabapentin is required to be given. You have 0.3g capsules. How many would you

give?

5 A patient is prescribed an injection of 80mg of pethidine. You have available 100mg in 1mL.

How much fluid would you draw up?

6 You have oral amitriptyline 10mg in a 5mL solution. The patient is prescribed 25mg. How

much do you administer?

7 The maximum dose of paracetamol is 4g in a 24-hour period. The tablets are 500mg. What

is the maximum number of tablets you can give in a 24-hour period?

8 A patient requires 4mg of intramuscular morphine sulphate. You have reconstituted the mor-

phine to make a dose of 10mg in 1mL. How much do you draw up?

9 35mg of codeine is to be given to a patient subcutaneously. You have available 50mg in

1mL. How much do you administer?

10 Fentanyl 75mcg is to be given intravenously. You have fentanyl 0.1mg in 1mL available. How

much would you draw up

Multiple-choice questions

Try answering these multiple-choice questions to test what you have learned from reading this

chapter. You can check your answers at the end of this book.

1. What is the role of prostaglandins in the reception of pain?

a) They make the nociceptors more sensitive

b) They directly stimulate the nociceptors

c) They stimulate the release of bradykinin

d) They only act on receptors in the central nervous system

2. Local anaesthetic agents work by …

a) Opening potassium channels

b) Opening sodium channels

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Chapter 4 Local anaesthetics and analgesics

c) Blocking potassium channels

d) Blocking sodium channels

3. Why are some local anaesthetics given with adrenaline?

a) Adrenaline is needed in order for local anaesthetics to work

b) Adrenaline counteracts the vasodilation caused by local anaesthetics

c) Adrenaline makes local anaesthetics work more quickly

d) Adrenaline helps the local anaesthetic enter the cells

4. NSAIDs work by …

a) Blocking production of bradykinin

b) Making the neurone fire more frequently

c) Stimulating the body’s own analgesic system

d) Blocking production of prostaglandins

5. Why is it important to tell a patient who has been prescribed paracetamol to be

careful when buying OTC medicines?

a) It could be expensive for them

b) You must only take paracetamol on its own

c) Paracetamol is often combined with cold and flu remedies

d) Paracetamol easily interacts with OTCs

6. Ibuprofen must be taken with caution if the patient is also taking lithium – why?

a) The patient may forget to take the medicine

b) It may increase the lithium level in the blood

c) It will make the lithium inactive

d) Ibuprofen also affects mood

7. One of the mechanisms of opiates is thought to be …

a) Blockage of calcium channels

b) Opening of calcium channels

c) Blockage of sodium channels

d) Opening of sodium channels

8. Which of the following channels are blocked by gabapentin?

a) Sodium

b) Potassium

c) Calcium

d) Chloride

→

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Chapter 4 Local anaesthetics and analgesics

Recommended further reading

Antimicrobials

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Chapter 5 Antimicrobials

Introduction

Part of the nurse’s role is to ensure that medicines

are administered appropriately. The Nursing and

Midwifery Council’s Standards for Pre-Registration

Nursing programmes published in May 2018 state

that education must

ensure that field-specific content in relation to

the law, safeguarding, consent, pharmacology

and medicines administration and optimisa-

tion is included for entry to the register in one

or more fields of nursing practice

This is backed up by the Standards of Proficiency

for Registered Nurses as follows:

Platform 2: Promoting health and preventing ill

health

2.12 protect health through understanding and

applying the principles of infection prevention

and control, including communicable disease

surveillance and antimicrobial stewardship

and resistance

The Global Burden of Disease Study of 2017 shows

that communicable (or infectious) disease is still

a major cause of death and disability through-

out the world. Many micro-organisms live either

inside or on the outside of the human body. These

can live harmlessly on the host or can cause dis-

ease. Other micro-organisms are present in the

external environment and are introduced into our

bodies when eating and drinking, breathing or on

physical contact.

Micro-organisms that live in or on our bodies

for the most part have a harmless relationship with

us and can be beneficial – for example, bacteria in

the GI system break down foodstuffs, allowing us to

absorb nutrients. Unfortunately, at times of vulnera-

bility these same organisms can cause infection and

damage. Other micro-organisms that are not nor-

mally present in the body attempt to invade our tis-

sues, causing damage that can be life-threatening.

Any invasion or abnormal growth pattern of

micro-organisms which causes our body to defend

itself is called an infection. A common example

would be respiratory infections – the inflammation

of the membrane that lines the respiratory tract

and associated structures.

Micro-organisms are categorized into four main

groups: bacteria, viruses, protozoa and fungi. Other

groups such as algae and parasitic infections will

not be considered here. Bacteria and fungi are capa-

ble of existing independently of their host, i.e. us.

Some protozoa and certainly viruses need the mech-

anisms from our cells in order to replicate and grow.

Learning objectives

After studying this chapter, you should be able to:

■ Describe a bacterial cell.

■ Explain the mode of action of a range of antibiotics used in practice settings.

■ Demonstrate an understanding of what unwanted effects antibiotics have on humans.

■ Discuss drugs that are used to treat tuberculosis.

■ Define what is meant by viral disease.

■ Describe the mode of action and side-effects of antiviral medicines.

■ Identify the three main causes of fungal infection.

■ Explain how antifungal medicines act.

■ Demonstrate an understanding of the links between the pharmacology of antimicrobial ther-

apies and the care given by the health practitioner.

■ Solve correctly a number of drug calculations with regard to antimicrobial medicines.

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Chapter 5 Antimicrobials

This chapter is designed to provide an introduc-

tion to some of the medicines used in combating

infections caused by micro-organisms. These drugs

are referred to as antimicrobials. The chapter

covers antibiotic therapy, antiviral therapy, anti-

protozoa therapy and, finally, antifungal therapy.

We provide examples of common drugs that you

are likely to encounter in your clinical practice.

Bacterial infection

Bacteria are classified into several types based on

their shape. When viewed through a microscope,

some look like rods and are called bacilli. Some

have a curved rod shape and are known as vibrio.

Others are round and are called cocci. Still others

have a spiral or corkscrew shape and are known

as spirilla or spirochetes. Bacteria are also catego-

rized by whether they take up a stain called gram

stain: bacteria that absorb this stain are termed

gram positive, while those that do not are gram

negative.

Whether or not a gram stain is taken up depends

on the thickness of the cell walls of the bacte-

ria. Gram-negative bacteria have a thin cell wall,

whereas the cell wall of gram-positive organisms

is much thicker and can absorb the stain.

Bacteria cells are different from those of

humans. Bacteria do not have a nucleus and so

are called prokaryotes. Animal (including human)

cells do have a nucleus and are called eukary-

otes. This and other differences between bacteria

and human cells is important, as antibiotics are

designed to target these differences, thus combat-

ting the bacteria while leaving our own cells with

little or no damage.

On the very outside of a bacterium is a wall

made largely from a sugar called peptidoglycan.

This is unique to prokaryotic cells. Beneath this

wall is a plasma membrane very similar to our

own that consists of a sandwich of phospholipids

and proteins. Together, the cell wall and plasma

membrane are called the bacterial envelope.

A bacterium contains cytoplasm which car-

ries similar organelles to our own. However, the

genetic material is arranged in one long strand

that floats around in the cytoplasm. A prokaryotic

cell does not have any mitochondria and energy

production is carried out in the plasma membrane

(see Figure 5.1).

Antibiotics are described as being bactericidal

(i.e. they kill bacteria) or bacteriostatic (i.e. they

prevent the growth and replication of the bacteria

so they do not multiply and they die after their nat-

ural cycle has elapsed). This gives the body’s nat-

ural defence mechanisms time to recognize and

deal with the infection. The distinction between

these two terms is not black and white because

in certain conditions a bactericidal antibiotic may

only have a bacteriostatic effect and vice versa.

Their spectrum of effects can be governed by

dosage, outside influences and the health of the

patient.

Selective toxicity is the ability of the antimi-

crobial to harm a pathogen (bacteria) without

harming our own cells. Therefore, when discuss-

ing selective toxicity in terms of an antibiotic,

health care practitioners are referring to the range

between the dose necessary to inhibit or destroy

the bacteria and the dose at which our own cells

become harmed. Thus, an antibiotic that is far

more toxic to the bacteria than our cells is said to

have a greater selective toxicity.

ANTIBIOTIC ACTIONS

Different antibiotics interfere with bacterial cell

processes in different ways and we will explore

each in turn.

Interference with folate

Folate is a vitamin required by both bacterial and

human cells. Bacteria must make their own folate

and cannot absorb it directly from the environ-

ment. Humans cannot make their own and must

obtain it from their diet or through a supplement

if needed.

A group of antibiotics called sulfonamides

exploit this unique ability of bacterial cells. Bac-

teria need a substance called para-aminobenzoic

acid (PABA) as a precursor to synthesize the folate

they need. Sulfonamides are structural analogues

of PABA and act as a competitive antagonist and

are taken up by the bacteria as a pseudo-precursor

preventing the synthesis of folate. In this way,

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