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Chapter 8 Drugs for respiratory conditions

138

Calculations

1. A patient requires oral theophylline at a dose of 10mg/kg twice daily. They weigh

25kg. Your stock tablets are 250mg. How many would need for a 28-day supply?

2. Seratide inhaler contains 3000mcg of salmeterol. It contains 60 doses. How much salmet-

erol is in each dose?

3. A child requires fluticasone 100mcg twice daily and is prescribed an inhaler with 50mcg per

dose. How many doses of this are required for the day?

4. Your mentor asks you to check a dose of medication for IV injection. The patient requires

aminophylline 50mg and the ampoule comes as 250mg in 10mL. How much should have

been drawn into the syringe?

5. Your patient is prescribed salbutamol tablets at a dose of 4mg three times per day. You only

have access to 2mg tablets for preparing a 7-day supply. How many will you need?

6. Your patient is prescribed indacaterol for COPD. They should take 150mcg daily for 4 days,

then increase the dose to 300mcg. Each dose in the inhaler contains 150mcg and there are

30 actuations. How long will this inhaler last?

7. A patient requires 125mcg of ipratropium by nebulizer. You have 500mcg in 2mL solution.

How much do you put into the nebulizer chamber?

8. Your patient has been prescribed a salbutamol ‘easyhaler’ which has 100mcg per dose and

200 doses per device. They can take the 100mcg up to eight times per day. How many

inhalers should be prescribed to guarantee a 30-day supply?

9. Roflumilast 500mcg tablets come in a pack of 30 costing £37.71. The patient requires 13

of these per year to cover all days of treatment. What is the annual cost of this drug??

10. Montelukast 4mg sachets cost £4.85 for 28 but the 4mg chewable tablets cost £0.89. How

much more expensive would it be for 13 prescriptions per year to give the granules?

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. Which of the following drugs is a beta 2 agonist used in the treatment of asthma?

a) Ipratropium

b) Salbutamol

c) Beclometasone

d) Theophylline

→

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Chapter 8 Drugs for respiratory conditions

139

2. What measures might be employed to help reduce the possibility of developing oral

candidiasis when using inhaled corticosteroids?

a) Using a spacer and altering the inhaler technique

b) Altering the inhaler technique and taking antifungal lozenges

c) Rinsing the mouth and altering the inhaler technique

d) Using a spacer and rinsing the mouth after taking the medication

3. Which of these drugs is a weak inhibitor of phosphodiesterase?

a) Theophylline

b) Salbutamol

c) Roflumilast

d) Fluticasone

4. Tiotropium is an example of which class of drug?

a) LABA

b) Corticosteroid

c) Anti-muscarinic

d) PDE4 inhibitor

5. Which of the following drugs acts at leukotriene receptors?

a) Salmeterol

b) Salbutamol

c) Montelukast

d) Fluticasone

6. Which drug group would be the first-line management of asthma after a short-

acting beta 2 receptor agonist is prescribed?

a) Long-acting beta-adrenoreceptor agonists

b) Inhaled corticosteroids

c) Leukotriene receptor antagonists

d) Oral corticosteroids

7. Fluticasone with salmeterol is an example of a combination of which two classes

of drug?

a) Corticosteroid + leukotriene receptor antagonist

b) Corticosteroid + short-acting beta 2 agonist

c) Corticosteroid + LAMA

d) Corticosteroid + LABA

→

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Chapter 8 Drugs for respiratory conditions

140

8. The most common cause of COPD is …

a) Previous diagnosis of asthma

b) Smoking

c) Air pollution

d) Genetic predisposition

9. Asthma diagnosis in children is difficult because …

a) It is a complex condition in the young

b) Children’s lungs are not mature

c) Children cannot perform spirometry

d) They often grow out of it

10. Which of the following are risk factors for childhood asthma?

a) Prematurity

b) Presence of atopic condition

c) Parents who smoke

d) All of the above

→

Recommended further reading

Drugs for diabetes mellitus

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Chapter 9 Drugs for diabetes mellitus

142

Introduction

In this chapter, you will learn about the two types

of diabetes and their similarities and differences.

Diabetes is a common condition across the UK

and the developed world. The Diabetes Prevalence

Survey of 2018 (Diabetes UK 2019) showed that

3.8 million people were diagnosed with diabetes in

the UK. These figures are extrapolated from the

Quality and Outcomes Framework (QOF) registers

compiled by general practices throughout the UK.

Part of the nurse’s role is the need 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 in the area of skills:

Annexe A: Communication and relationship

management skills

2. Evidence-based, best practice approaches to

communication for supporting people of all

ages, their families and carers in preventing

ill health and in managing their care

2.1 share information and check understand-

ing about the causes, implications and treat-

ment of a range of common health conditions

including anxiety, depression, memory loss,

diabetes, dementia, respiratory disease, car-

diac disease, neurological disease, cancer, skin

problems, immune deficiencies, psychosis,

stroke and arthritis

Diabetes

Diabetes mellitus is a chronic disease of metabo-

lism caused by either an insufficient production of

insulin in the body or an insufficient effect of insu-

lin in the peripheral tissues. The main problems

stem from a wide fluctuation in the range of blood

glucose levels, which leads to several short- and

long-term difficulties for the individual. There

are two main forms of diabetes: type I and type II

(see Box 9.1).

→

Box 9.1 The two types of diabetes

Type I Type II

Description Little or no insulin is

produced by the pancre-

as; insulin is required

to sustain life, thus the

need for daily insulin in

order to survive

Pancreas doesn’t make

enough insulin, or body

doesn’t use insulin correctly,

thus the need to control the

intake of carbohydrates.

Some people can maintain

normoglycaemia with diet

alone, some need oral

hypoglycaemic drugs, while

some will eventually require

insulin

Usual age of onset Less than 20 years Typically, 40–60 years

Control by oral antidiabetic drugs No Possible

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Chapter 9 Drugs for diabetes mellitus

143

In type I diabetes, the body produces little or no

insulin in cells contained in the pancreas known

as the ‘Islets of Langerhans’ or the beta cells. The

pancreas is a specialized gland that lies just behind

the stomach. Its functions range from regulating

the amount of sugar (glucose) in the blood to pro-

ducing enzymes that help break down and digest

proteins, carbohydrates and fats. It is thought that

the beta cells in the pancreas are destroyed by the

body’s own immune response – hence diabetes is

an autoimmune disease. Someone with type I dia-

betes will be required to take insulin for the rest of

their lives.

In type II diabetes, the beta cells may produce

small amounts of insulin but not enough to control

the levels of glucose in the plasma. In addition, the

cells of the body, and particularly in the periphery,

cannot utilize insulin properly. This means that

glucose is stopped from entering peripheral cells,

so increasing the glucose levels in the plasma. This

type of diabetes is linked to the problem of obesity.

As stated in the Introduction, an estimated

3.8 million people in the UK are currently living with

diabetes (Diabetes UK 2019). However, it is sug-

gested that there are as many people again who go

undiagnosed. The figures suggest that around 90%

those diagnosed have type II diabetes, 8% have

type I and around 2% have rarer types of diabetes.

The risk of type II diabetes is higher if it runs

in the family or if the patient is overweight. From

Control by insulin Yes May be required as the

disease progresses or if the

patient remains unresponsive

to oral therapy

Symptoms Symptoms appear rapidly:

frequent micturition;

extreme hunger; extreme

thirst; extreme weight

loss; weakness and tired-

ness; feeling edgy and

mood changes; nausea;

vomiting; blurred vision

Symptoms appear slowly

(the person may not feel any

symptoms at all): increased

thirst; increased micturition;

feeling tired; feeling edgy;

nausea; loss of weight; slow

wound healing; recurrent

infections of the skin, gums,

vagina/penis and bladder;

blurred vision; tingling or loss

of sensation in hands or feet

Complications Diabetic coma or keto-

acidosis from hypergly-

caemia; hypoglycaemia;

nephropathy; blindness;

myocardial infarction;

cerebrovascular accident;

peripheral vascular dis-

ease; neuropathy

Diabetic coma from hyper-

glycaemia; hypoglycaemia;

nephropathy; blindness;

myocardial infarction; cerebro-

vascular accident; peripheral

vascular disease; neuropathy

Treatment Carbohydrate-controlled

healthy diet; exercise;

daily insulin; regular mon-

itoring of blood glucose

levels; monitoring of urine

Carbohydrate-controlled

healthy diet; exercise; regular

monitoring of blood glucose

levels; monitoring of urine

→

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Chapter 9 Drugs for diabetes mellitus

144

this perspective, prevention of obesity will also

lead to prevention of type II diabetes.

Without treatment, the main symptoms of dia-

betes can be divided into two main types: acute

symptoms and chronic complications. There are a

number of symptoms that could be referred to as

‘classic’. These are excessive thirst (polydipsia),

producing lots of urine requiring many trips to the

bathroom (polyuria), blurring of vision, tiredness

and weight loss due to muscle wasting (loss of

muscle mass).

The chronic complications of diabetes are

caused by long-term raised glucose levels in the

body. This leads to damage, particularly to blood

vessels and peripheral nerves.

death. DKA, therefore, will be diagnosed with the

detection of ketosis and metabolic acidosis in the

presence of hyperglycaemia. Treatment of DKA

involves replacing fluids, administrating insulin

and preventing the patient’s potassium levels from

dropping (hypokalaemia).

As we have indicated, DKA is most common

among patients with type I DM and develops

when their ability to produce insulin is insuffi-

cient to meet the body’s basic metabolic require-

ments. In a small minority of patients, DKA is the

first indication of type I DM. Insulin deficiency

can be described as absolute, such as when a

patient does not administer their insulin. Insulin

deficiency can also be described as relative, such

as when the usual level of insulin is not enough to

meet the body’s metabolic demands from physi-

ological stress. Stressors that can cause this rel-

ative imbalance and cause DKA include acute

infection such as pneumonia or the development

of a urinary tract infection. Myocardial infarction

is another complication that can trigger DKA.

Certain drugs are also implicated in causing DKA,

including corticosteroids, thiazide diuretics and

sympathomimetics.

In type II diabetes, DKA is less common, but it

can occur in individuals under abnormal physio-

logical stress.

Treatment

The management of DKA involves the replace-

ment of fluid and electrolytes and the administra-

tion of insulin. Such management should follow

the Guidelines for the Management of Diabetic

Ketoacidosis in Adults (2013), published by the

Joint British Diabetes Societies Inpatient Care

Group. Such treatment should ideally be given

in high-dependency settings because clinical and

laboratory assessments are at first required every

1–2 hours, with appropriate adjustments in treat-

ment.

Intravenous fluids are needed immediately, as

intravascular volume should be restored in order

to raise blood pressure and therefore ensure kid-

ney perfusion. Once this immediate intravenous

fluid has been given, the team needs to ensure

Clinical tip

Macrovascular disease refers to dam-

age to the larger blood vessels resulting in

coronary heart disease or peripheral vascular

disease. Microvascular disease, in contrast,

refers to damage to smaller vessels resulting

in eye problems (retinopathy) and kidney

damage (nephropathy). Damage to the out-

side of the nerves (the nerve sheaths) is also

a problematic complication; this process is

referred to as ‘neuropathy’, a major cause of

diabetic foot problems including amputation.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a complication

of diabetes. A patient with DKA will have high

blood glucose levels (hyperglycaemia), high lev-

els of ketone bodies in their plasma (ketosis),

and because these ketone bodies are acidic, the

patient’s blood becomes more acidic (metabolic

acidosis). DKA occurs mostly in people with type I

diabetes mellitus (DM).

The patient often reports feeling nauseous

and may actually start to vomit. Another com-

mon symptom is abdominal pain. If these signs

and symptoms are left unchecked, the condition

can progress to cerebral oedema, coma, even

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Chapter 9 Drugs for diabetes mellitus

145

that the remaining total body water deficits are

corrected more slowly. This may take place over

the next 24 hours. When blood pressure is over

90mmHg, sodium chloride 0.9% should be given by

intravenous infusion at a rate that addresses the

deficit and provides maintenance; see Joint British

Diabetes Societies Inpatient Care Group (2013) for

suggested regimen.

The usual way to correct hyperglycaemia is

to give the patient regular insulin, such as insulin

detemir or insulin glargine. Initially, the patient

may require 0.1 unit/kg as an IV bolus of soluble

insulin. This is then followed by a continuous IV

infusion of 0.1 unit/kg/hour in 0.9% saline solution.

During this time the patient’s blood sugar will be

regularly monitored. If the plasma concentration

of glucose does not fall by 50 to 75mg/dL (2.8 to

4.2mmol/L) in the first hour, insulin doses should

be doubled. Children should be given a continuous

IV insulin infusion of 0.1 unit/kg/hour or higher

with or without a bolus.

If the doses of insulin are sufficient, you should

begin to see an improvement in the levels of cir-

culating ketones. Sometimes an improvement in

ketosis is linked to an improvement in the pH of

the blood. This means that ketone decline may

take some time until the blood pH improves.

As the patient’s condition improves, attention

will turn to the type of insulin to be given next.

The patient will be switched to regular insu-

lin 5–10 units every 4–6 hours, with the route of

administration being by subcutaneous injection.

When the patient’s condition has been stabilized

and they are able to eat and drink normally, a typ-

ical split-mixed or basal-bolus insulin regimen is

begun. During this transitional period, the patient

should continue intravenous insulin for 1–4 hours

after the initial dose of subcutaneous insulin is

given. In contrast, children should continue to

receive 0.05 unit/kg/hour insulin infusion until sub-

cutaneous insulin is initiated and pH exceeds 7.3.

Hypokalaemia, or low potassium levels, needs

to be prevented. This occurs in DKA because of

urinary loss. Prevention requires close monitoring

and replacement of potassium, which will be given

alongside the patient’s intravenous fluids. Levels

should be checked every 1–2 hours in the initial

stages of treatment.

Medicine management of diabetes

The overall aim of the treatment of diabetes is

to maintain blood glucose levels within the nor-

mal range (normoglycaemia) and achieve the

required HBA1c target for the patient based on

their condition and in line with guidelines. The

HBA1c measurement gives an understanding of

the diabetic control over the past 8–12 weeks and

is a better indicator for the prescriber than a spot

blood glucose check. This will relieve the acute

symptoms and should minimize the impact of

chronic complications on the individual. Achiev-

ing normoglycaemia is very difficult and drug

treatment is on an individual basis. An increase in

exercise and cessation of smoking are advisable

in order to reduce high blood pressure (hyperten-

sion) and high fat content in the blood (hyper-

lipidaemia). These measures have been shown

to reduce the risk of long-term complications of

this disease. However, the most important key

to treatment of diabetes is diet. This can be done

alone or in combination with insulin or other oral

hypoglycaemic agents.

Insulin

The hormone insulin is released in the body as a

direct response to raised levels of blood glucose.

Insulin is released directly into the bloodstream

and stimulates the uptake of glucose; it is the key

that allows glucose to enter cells, and without it

the door remains locked and glucose builds up in

the blood. Insulin also promotes conversion of glu-

cose to a substance called glycogen, which allows

the body to store glucose for periods when the

person is not eating but still requires glucose for

bodily functions.

Insulin also limits the amount of fat breakdown

in the body, a process called lipolysis. Triglyc-

erides (large fat molecules), which are normally

stored in fatty (adipose) tissue, are broken down

into their constituent fatty acids and glycerol.

These are then transported to the liver where

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Chapter 9 Drugs for diabetes mellitus

146

they are used to fuel certain metabolic pathways.

As insulin is either absent or low in quantity in

diabetes, these metabolic pathways soon become

saturated, resulting in the production by the body

of acidic compounds such as ketone bodies and

acetate.

Treatment with insulin

At one time, insulin was extracted from the pan-

creas of cattle (bovine insulin) or pigs (porcine

insulin). However, today it is almost entirely

human in nature. This is possible through use

of a process called recombinant DNA technol-

ogy, which involves inserting the DNA code for

human insulin production into bacteria so that

they then produce commercial amounts of insu-

lin (see Box 9.2).

Insulin is destroyed in the GI system, which is

why you never see it given by mouth as a tablet,

for example.

Once absorbed, insulin has a short half-life of

approximately 10 minutes. Therefore, for longer-

term control, long-acting insulin is required.

Insulin doses need to be drawn up precisely and

injected subcutaneously at times determined by

the prescriber in line with the patient’s lifestyle

and needs. Insulin doses can be varied in line with

blood glucose readings.

Rapid-acting insulins

Soluble insulin produces a quick and short-lived

effect. It works in the same way as natural insulin

by binding to the receptors on the cells and allow-

ing glucose to enter. It also causes the cells in the

liver, muscles and fat to increase their uptake of

glucose from the blood. Insulin lispro is a special

form of human insulin that works more rapidly but

for a shorter period of time. This enables people to

inject themselves just prior to eating a meal if they

Clinical tip

Insulin is usually given by injection.

The most common method of administra-

tion is subcutaneously. It can be auto-

injected by means of a device called a

‘pen’, although some patients prefer to

use a small insulin pump. The most recent

device available is the insulin jet system,

which can be used on the abdomen, thighs

or buttocks. It forces a very small stream of

insulin through a nozzle placed on the skin.

The jet of insulin is propelled with such

force that it penetrates the skin without the

need for a needle.

Box 9.2 Types of insulin

Rapid-acting analogue (clear)

Onset: 10–15 minutes

Peak: 60–90 minutes

Duration: 4–5 hours

Fast-acting (clear)

Onset: 30 minutes–1 hour

Peak: 2–4 hours

Duration: 5–8 hours

Intermediate-acting (cloudy)

Onset: 1–3 hours

Peak: 5–8 hours

Duration: up to 18 hours

Long-acting (cloudy)

Onset: 3–4 hours

Peak: 8–15 hours

Duration: 22–26 hours

Extended long-acting analogue

Onset: 90 minutes

Duration: 24 hours

Premixed (cloudy)

Presented as a single vial containing a fixed

ratio (a percentage of rapid-/fast-acting to a

percentage of intermediate-/long-acting)

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Chapter 9 Drugs for diabetes mellitus

147

so wish. These types of insulins are the only ones

suitable for IV injection.

insulin aspart and biphasic insulin lispro. Pre-

mixed combinations provide a rapid initial lower-

ing of blood glucose, followed by a more prolonged

effect that lasts throughout the day. This is thought

to mimic the body’s own insulin production more

closely.

Long-acting insulins

Like intermediate-acting insulins, long-acting insu-

lins (examples of which include protamine zinc

insulin, insulin zinc suspension, insulin detemir,

insulin glargine and insulin degludec) function

like the body’s normal insulin production, but their

duration of action may last up to 36 hours. Insu-

lin glargine and insulin degludec are given once

daily and insulin detemir is given once or twice

daily according to individual requirements. The

older long-acting insulins (insulin zinc suspen-

sion and protamine zinc insulin) are rarely pre-

scribed these days.

Side-effects

The main problem when giving insulin is that the

blood sugar may be lowered too much, a state we

call hypoglycaemia, which can cause brain dam-

age. A person using insulin is three times more

likely to be at risk from the effects of hypoglycae-

mia than a non-user.

Clinical tip

Examples of rapid-acting soluble insu-

lins include insulin aspart, insulin glulisine

and insulin lispro. When given subcutane-

ously, they work within 30–60 minutes with

a peak action between 1 and 4 hours, and

their effects last for around 9 hours. They

are usually injected 15–30 minutes before

a meal so that the increasing blood glucose

levels after eating can be controlled. You

will see these sorts of insulins being used

in clinical practice as treatment for ketoac-

idosis where the regime is also called a

‘sliding scale’. This means the insulin dose

is determined by the person’s blood glucose

value, which is obtained at predetermined

times (e.g. every 2 hours).

Clinical tip

Isophane insulin is naturally white and

cloudy in appearance and should not be used

if it is not uniformly this colour after mixing.

To mix the vial, gently roll it in your hands at

least 10 times before administration.

Clinical tip

Patients with hypoglycaemia become

dizzy, feel faint, begin to sweat and often

appear to be drunk. The obvious way to

treat this is to give sugar in the form of

sweet drinks, glucose tablets or sugary

snacks. If the person is unconscious, and

this can occur relatively quickly, they will

need IV glucose or intramuscular gluca-

gon. Glucagon is a hormone that works

in the opposite way to insulin and raises

the blood glucose level by promoting the

breakdown of stored glucose in the liver

and muscles.

Intermediate-acting insulins

Longer-acting preparations of insulin are made

possible by mixing the insulin with a substance

that slows its use in the body. An example of this

is isophane insulin, which starts working about

90 minutes after administration. Its maximum

effect occurs 4–8 hours after administration and

keeps working for as long as 24 hours.

The biphasic insulins are a combination of

soluble insulin and isophane insulin. Examples of

these include biphasic isophane insulin, biphasic

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