CHAPTER 26: Chronic Obstructive Pulmonary Disease
Characterized by airflow limitation that is not
fully reversible.
Airflow limitation is usually both progressive and
associated with an abnormal inflammatory
response of the lungs to noxious particles or
gases.
It is a general term that covers variety of other
disease labels
Chronic obstructive lung disease (COAD)
Chronic obstructive airways disease
(COLD)
Chronic Bronchitis or Emphysema
Airflow obstruction with a reduced FEV1/FVC
ratio of >80% of predicted normal, a diagnosis of
COPD should only be made in the presence of
respiratory symptoms (breathlessness or cough)
Respiratory disease including chronic bronchitis
are more common in areas:
high atmospheric pollution
In people with dust occupations (foundry
workers and coal miners)
Highly industrialized- highest incidence
of COPD
PATHOLOGY
Affect 4 different compartments of the lung and
all are affected in most individuals to varying
degrees.
Central airways (< 2mm diameter, Cartilaginous)
Bronchial glands hypertrophy and goblet cell
proliferation occurs.
Results in excessive mucus production
(Chronic bronchitis)
Chronic Bronchitis
- Defined as a chronic or recurrent
cough with sputum production on
most days for atleast 3 months of the
year during atleast 2 consecutive
years.
- There is a loss of ciliary function with
increase in inflammatory cells
(lymphocytes, macrophages, and
later in disease, neutrophils).
Peripheral airways (< 2mm diameter, non-cartilaginous)
Bronchiolitis is present from early disease with a
pathological increase in goblet cells in
inflammatory cells in the airway walls.
With disease progression, fibrosis develops along
with an increase of collagen in the airway walls.
Lung Parenchyma (respiratory bronchioles, alveoli and
capillaries)
In emphysema:
Elastases destroy elastin resulting in
dilation and destruction of the
respiratory bronchioles and alveolar sacs
and ducts.
There is a loss of the alveolar wall
attachments and peripheral
airway.
Emphysema- abnormal enlargement of the air
spaces distal to the terminal bronchioles
FORMS:
1. Centrilobular emphysema
o Dilation and destruction of the
respiratory bronchioles and
alveolar sacs and ducts.
o Predominates in COPD
2. Panacinar emphysema
o Destruction of the whole acinus
o Predominates in patients with
- antitrypsin deficiency
Pulmonary vasculature
Vessel walls thicken in the course of diseases
along with endothelial dysfunction.
Vessel walls become infiltrated by inflammatory
cells (macrophages and lymphocytes)
There is an increased vascular smooth muscle
w/c can lead to pulmonary HTN.
Advanced disease: there is an emphysematous
destruction of the vascular bed and collagen
deposition.
ETIOLOGY Inflammation
COPD is characterized by chronic inflammation
Tobacco smoking
throughout the airways, parenchyma, and
Most important and dominant risk factor in the pulmonary vasculature.
development of COPD but other noxious particles Increase neutrophils, macrophages and T-
also contributes (chemical fumes, irritants, dust lymphocytes (CD8+)
and gases). Increase eosinophils- during exacerbation
A persons exposure can be thought of in terms Cause release of inflammatory
of the total burden of inhaled particles. mediators and cytokines such as:
Leukotriene B4
Cause (normal) inflammatory response in the
Interleukin-8
lungs.
Tumor necrosis factor-
Cause tissue destructions and impaired repair
Damages by lungs.
mechanism due to the exaggerated response of
Proteinases and antiproteinases imbalance
the smokers.
1-antitrypsin-deficient are individuals are at
Imbalance proteinases and antiproteinaces in the
increased risk of emphysema
Oxidative stress
Lead to imbalance between proteinases and
antiproteinases.
PATHOGENESIS OF COPD o Lead to lung destruction
In COPD
Increased production/ activity of proteinases
Inflammation Proteinaces and Oxidative stress
Decreased production/ activity of
antiproteincaes
antiproteinases.
imbalance
The main proteinases, proteolytic enzymes
(neutrophil elastin) are released by macrophages
Risk:
and or neutrophils.
Genetic factors
Age ( at w/c individual begins smoking) The antiproteinases inhibit the damage caused by
Total pack years the proteolytic enzyme.
Current smoking status 1- antitrypsin or 1 proteinase
Natural aging process of the lungs inhibitor- main antiproteinases
Male (chronic bronchitis) o Inactivated by cigarette smoke
Occupation o Decrease by oxidative stress
Pollution
Socio economic status Oxidative stress
Airway hyper-responsiveness and allergy Imbalance of oxidants and antioxidants exist in
Passive exposure to cigarette smoke may also COPD with the balance in favor of oxidants.
contribute to respiratory symptoms and COPD by Contributes to the development of the disease
increasing the lungs total burden of inhaled by:
particles and gases. Damaging the intracellular matrix
Tobacco exposure is quantified in pack years Oxidizing biological molecules- cause cell
destruction
No. of cigarettes Promoting histone acetylation
Total pack years = smoked per day X no. of There is a link between oxidative stress and the
20 yrs. Of smoking poor response to corticosteroid seen in COPD.
Corticosteroid must recruit histone
deacetylase to switch off the
transcription of inflammatory genes.
 In COPD, the activity of histone deacetylase is
impaired by the oxidative stress
Reducing the responsiveness to
corticosteroids.
Cigarette smoke also impairs the function of
histone deacetylase.
PATHOPHYSIOLOGY
Physiological abnormalities of COPD
Mucus hypersecretion
Ciliary dysfunction
Airflow limitation and hyperinflation
Gas exchange abnormalities
Pulmonary HTN
Systemic effects
Mucus hypersecretion, ciliary dysfunction and
complication
Enlarged mucus glands
Cause:
Hypersecretion
Squamous metaplasia of epithelia cells
Results: Ciliary dysfunction
1st physiological abnormalities in COPD
Cilia and mucus- protects against inhaled
irritants w/c are trapped and expectorated.
Cigarette smoke
Cause persistent irritation
exaggeration in the response of these
protective mechanism inflammation of
the small bronchioles (bronchiolitis) and
alveoli (alveolitis)
Inhibits mucociliary clearance causes
further build up of mucus in the lungs.
Macrophages and neutrophils
infiltrate the epithelium and
trigger a degree of epithelial
destruction.
o Together with
proliferation of mucus
producing cells , leads to
plugging of smaller
bronchioles and alveoli
with mucus and
particulate matter
Excessive mucus production distension of the
alveoli and loss of their gas exchange function
Pus and infected mucus accumulate,
leading to recurrent or chronic viral and
bacterial infections.
Primary pathogen- usually viral but bacterial
infection often follows.
Common bacterial pathogens
Streptococcus pneumoniae
Moraxella catarrhalis
Haemophilus influenzae
Bronchiectasis
A pathological change in the lungs where
the bronchi become permanently dilated.
Common after early attacks of acute
bronchitis during w/c mucus both plugs
and stretches the bronchial walls.
In severe infections, the bronchioles and
alveoli can become permanently
damaged and do not return to their
normal size and shape.
The loss of muscle tone and loss of cilia can
contribute to COPD because mucus has a
tendency to accumulate in the dilated bronchi.
Airflow limitation and hyperinflation
Main site: Fibrosis and narrowing (airway
remodeling) of the smaller conducting airways
(<2mm diameter).
Compounded by:
Loss of elastic recoil (destruction of
alveolar walls)
Destruction of alveolar support/
attachments
Accumulation of inflammatory cell mucus
and plasma exudates
Spirometry- measures the degree of airflow
limitation
Emphysema- progressive destructive
enlargement of the respiratory bronchioles,
alveolar ducts, and alveolar sacs.
2 main consequences of adjacent alveoli:
1. Loss of available gas exchange surfaces
increase in dead space and impaired gas
exchange
 2. Loss of elastic recoil in the small airways, vital Dilation and progressive right ventricular
for maintaining the force of expiration, w/c failure (cor pumonale)
leads to a tendency for them to collapse Pulmonary edema- physiological changes
during expiration particularly. subsequent to the hypoxemia and
Increase thoracic gas volume and hyperinflation hypercapnia
of the lungs. o activation of renin-
BOX 26.1 angiotensin system
o salt and water retention
Gas exchange abnormalities o reduction in renal blood
Occurs in advanced disease flow
Characterized by arterial hypoxemia with or
Systemic effects
without hypercarbia.
Abnormal distrib1ution of ventilation and Systematic inflammation and skeletal wasting
perfusion within the lungs and create the limit exercise capacity and worsen prognosis.
abnormal gaseous exchange. (COPD) Consequence/sequelae:
Pulmonary HTN and cor pulmonale Osteoporosis
Develops in COPD after gas exchange Depression
abnormalities have developed. Normocytic and normochromic anemia
Thickening to bronchiole and alveolar walls Increase risk of cardiovascular disease
resulting from chronic inflammation and edema Elevated levels of C-reactive protein
leads to blockage and obstruction of the airways.

Alveolar distension and destruction

Distortion of blood vessels associated with

alveoli.

Increase BP in pulmonary circulation

Reduction of in gas diffusion across the alveolar

epithelium low partial pressure of oxygen in
the BV (Hypoxemia) due to an imbalance
between ventilation perfusion.
Chronic vasoconstriction increase in BP
compromise gas diffusion from air spaces into the
bloodstream.
Chronic low oxygen levels polycythemia
increase blood viscosity
In advanced disease, persistent hypoxemia
develops along with pathological changes in the
pulmonary circulation.
Sustained pulmonary HTN thickening of the
walls of the pulmonary arterioles associated with
pulmonary remodeling and increase in right
ventricular pressure within the heart.
Consequence of high right ventricular pressure
Right ventricular hypertrophy
CLINICAL MANIFESTATION
Diagnosis
A diagnostic COPD should be considered in any
patient who has symptoms of :
Cough
Wheeze
Regular sputum production or exertional
dyspnea
Or a history of exposure to COPD
Spirometry- confirm the diagnosis
Clinical features
Progressive disorder
Clinical features:
Bronchitis
Emphysema
Chronic bronchitis
Exhibit excess mucus production and degree of
bronchospasm resulting in wheeze and dyspnea
Hypoxia and hypercapnia (high levels of carbon
dioxide)
Has a productive cough
Overweight
Physical exertion is difficult due to dyspnea
Sometimes referred to as blue bloater
Blue bloater- tendency of the patient to retain
carbon dioxide caused by a decrease
responsiveness of the respiratory centre to prolong
hypoxemia that leads to cyanosis and peripheral
edema.
Lose the ability to increase the rate and depth of
ventilation in response to persistent hypoxemia
Decrease ventilator drive abnormal
peripheral or central respiratory receptors.
Increasing frequency of exacerbations of acute
dyspnea triggered by excess mucus production
and obstruction as the disease progress.
In severe cases
Chest diameter is often increased,
giving classic barrel chest.
As obstruction worsens,
hypoxemia increases pulmonary
HTN
Right ventricular strains leads to right ventricular
failure.
Right ventricular failure
Characterize by jugular venous
distension
Hepatomegaly
Peripheral edema
** All of w/c are consequence of increase in
systemic venous BP
Recurrent lower respiratory tract infections can
be severe and debilitating
Signs:
Increase in volume of thick and viscous
sputum (yellow or green and may
contain bacterial pathogens)
Squamous epithelial cells
Alveolar macrophages and saliva
Pyrexia may not be present
Cardiorespiratory failure with hypercapnia occurs
eventually severe, unresponsive to treatment
result to death.
Emphysema
Increasing dyspnea even at rest
Minimal cough
Sputum produced is scanty and mucoid
Bronchial infections is less common
Referred to a pink puffer
Pink puffer- hyperventilates to compensate for
hypoxia by breathing in short puffs.
- The patient appears pink with little
carbon dioxide retention and little
edema.
Breath rapidly (tachypnea)- respiratory centres
are responsive to mild hypoxemia and will have a
flushed appearance
Patient is thin and has pursed lips in an effort to
compensate for a lack of elastic recoil and exhale
a large volume of air.
Hypoxemia is not a problem unless the disease is
progressing.
 Progressively dyspnoeic, without exacerbation
triggered by increased sputum production.
Cor pulomale will develop eventually.
Leading to intractable hypercapnia and
respiratory arrest
2 ends of COPD
Blue bloater
Pink puffer
Additional specific problems
Obstructive sleep apnea hypoapnea syndrome
(OSAHS)
Acute respiratory failure
Sleep apnea syndrome
Frequent or prolonged pauses in breathing
during sleep deterioration in arterial blood
gases and decrease in the saturation of Hgb
with O2
Hypoxemia
Accompanied by pulmonary HTN and cardiac
arrhythmias premature cardiac failure
Acute respiratory failure
Occurred if the PaO2 suddenly drops and
there is an increase in PaCO2 that decreases
the pH to 7.3 or less.
Most common cause is acute exacerbation of
chronic bronchitis with an increase in volume
and viscosity of sputum.
Impairs ventilation and causes more severe
hypoxemia and hypercapnia.
Signs and symptoms:
Restlessness
Confusion
Tachycardia
Cyanosis
Sweating
Hypotension
Eventual unconsciousness
INVESTIGATIONS
Lung function test- assists in diagnosis
Spirometer- measure lung volumes and flow rates and
categorise the severity of COPD.
Forced expiratory volume in the firs second of
exhalation (FEV1) - main measurement
Other test:
Vital capacity (VC) - volume of air inhaled and
exhaled during maximal ventilation.
Forced vital capacity the volume of air inhaled
and exhaled during a forced maximal expiration
after full inspiration.
Residual volume (RV) the volume of air left in
the lungs after maximal exhalation.
Airflow obstruction
FEV1 less than 80% of that predicted for the
patient
FEV1/FVC less than 0.7
Bronchitis Emphysema
VC Decrease Decrease
RV Increase Increase (higher)
Total lung Normal Increased
capacity
RV increases in emphysema due to air being
trapped distal to the terminal bronchioles as well
as in total lung capacity.
Smoking increases the normal deterioration in
FEV1 over time from about 30 mL/yr to 45mL/yr.
FEV1 and FVC detect changes in airways greater
than 2mm in diameter.
<2mm:
10-20% of normal resistance to flow
Severe obstruction
Extensive damage to the lungs by the
time LFT detect abnormalities.
LF deteriorate with age even in the absence of
COPD
Use of FEV1/FVC overdiagnosis in the elderly
And underdiagnosis in patients under 45 years
old.
 Testing should be carried out after a dose of
inhaled bronchodilator to prevent diagnosis or
overestimation of severity.
Chest radiographs
Reveal differences between the 2 disease
states.

Emphysema

Flattened diaphragm with loss of peripheral

vascular markings
Appearance of bullae
Indicative of extensive trapping of air.

Bronchitis

Increased bronchovascular markings

Cardiomegaly with prominent pulmonary
arteries.

Table 26.3

Table 26.4
TREATMENT
Stable COPD
Long acting oxygen therapy
Patient with severe COPD and hypoxemia
Box 26.2
Box 26.3
Most patient with COPD are considered to have
irreversible obstruction, in contrast to patients
with asthma, but significant number do seem to
respond to bronchodilators.
Smoking cessation
Smoking is the most important factor in
the development of obstructive airways
disease.
All patient should be encouraged to stop
smoking
If contraindicated, all patient who are
planning to stop smoking should be
offered:
Nicotine Replacement therapy
(NRT)
Varenicline
Bupropion
Brochodilators
Use to reverse airflow limitation
Respiratory function test- assesses
effectiveness.
Patient may experience improvement in
exercise tolerance or relief of symptoms
(wheeze and cough).
Initial empiric therapy with SABA-
prescribed when required, for the relief
of breathlessness and exercise limitations
are recommended for initial use.
If patient remain breathlessness or have
exacerbations despite SABA then
maintenance therapy is recommended
with:
FEV1 > 50% predicted: LABA or
LAMA
FEV1 <50% predicted: a
combination of either LABA and
ICSs or LABA and LAMA
Triple therapy- if the patient remains
breathless or has exacerbations.
Short acting bronchodilators (Short- acting B2 receptor
agonist or short acting antimuscarinic)
Rapid relief
Low incidence of SE
Inhaled treatment is as efficacious as oral agents.
There is a little benefit in giving more than 1 mg.
Effect lasts for 4 hours and they should be used
as required for symptom relief.
Used before exercise to improve exercise
tolerance.
In COPD, parasympathetic (vagal) airway muscle
tone is the major reversible component.
o Inhaled anticholinergic drugs- reverse
this vagal tone and have a bronchodilator
effect.
Long acting bronchodilators
Include LAMAs and LABAs.
Tiotropium
o Has a 24-h duration of action
o Reduce exacerbation rates
o Increase exercise tolerance
o Reduce rated of hospital admission.
High dose bronchodilators
Patient with distressing and debilitating
breathlessness despite maximal inhaled therapy
may benefit from higher doses ( inhaler or via
nebuliser)
Patient should have their initial therapy
optimized.
Theophylline
Weak bronchodilator but useful in physiological
effects in COPD
Increase respiratory drive
improve diaphragmatic function
improved CO
The use should only be considered after a trial of
short-acting with long-acting bronchodilators.
Initial therapeutic trial of several weeks should be
carried out.
 Persistent nocturnal symptoms (cough or
wheeze)- night time used of long acting
theophylline.
Factors that affects its clearance:
Cigarette smoking
Viral pneumonia
Heart failure
Concurrent drug treatment (macrolides)
It is being investigated in low concentrations for
its ability to reverse the decrease in histone
deacetylase activity associated with oxidative
stress.
Benefit in reversing corticosteroid resistance.
Corticosteroid
Patient with COPD has a poor response to
corticosteroids.
Have a largely steroid-resistant pattern of
inflammation.
It is postulated that the oxidative stress of COPD
inhibits the mechanism by w/c corticosteroid,
acting through histone deacetylase, switch off
activated inflammatory genes.
Long term benefits:
o With moderate-to-severe disease
o With an FEV1 <50%
o Who are having exacerbations requiring
treatment with antibiotics and oral
corticosteroids.
There is a reduction in the number of
exacerbation
o Increased risk of pneumonia
There is no inhaled steroid is licensed for use in
COPD except when used with LABA in
combination devices.
Oral steroids in stable COPD.
Maintenance oral therapy-
o If oral steroids cannot be withdrawn after
a short course prescribed to treat an
exacerbation.
o Lowest dose should be used.
The patient should always assess for
osteoporosis and the need for osteoporosis
prevention.
Patient over 65 years receiving maintenance
therapy automatically receive prophylactic
treatment for osteoporosis.
Mucolytics
Benefit in stable COPD if there is a chronic cough
productive of sputum.
Antibiotics and immunization
Prophylactic antibiotics have no place in the
management of COPD.
Vital if patient develops purulent sputum
For acute infective exacerbations of bronchitis
o Supply of antibiotics to keep at home to
start at the 1st sign of an exacerbation.
Initial routine sputum cultures
o Unreliable in identifying the pathogenic
organism.
Normal pathogens:
S. pneumonia
H. influenzae
M. catarrhalis
Usual antibiotics used:
Co-amoxiclav
Amoxicillin
Erythromycin
Doxycycline
If the infection follows influenza, Staphylococcus
aureus may be present
o Antistaphylococcal agent (Flucloxacillin)
Sputum Cultures
o If the infection is considered atypical in
presentation or if the purulent sputum is
still present after 1 week of treatment.
o Identify pathogenic organisms
Reduce hospitalization and the risk of death in
the elderly with chronic lung disease and should
be offered to those with chronic airflow
obstruction.
o Single dose of pneumococcal vaccine
o Annual influenza vaccinations
Acute exacerbations of COPD
Acute worsening of the disease.
This exacerbation can be spontaneous but are
often precipitated by infection and lead to:
Respiratory failure with hypoxemia
Retention if carbon dioxide
Bronchodilators
Treat the increased breathlessness that is
associated with exacerbations.
Can be given by metered-dose inhaler (MDI) or
nebuliser.
B2- agonist can be given with or without an
anticholinergic agent.
Antibiotics
Treat exacerbation of COPD associated with a
history of more purulent sputum.
Choice of antibiotics is dependent on:
Local policy
Sensitivity pattern
Previous treatments
First line agent:
o Aminopenicillin
o Macrolide with increased activity against
H. influenzae or oxytetracycline
Corticosteroids
Short course of oral steroids
o Benefit FEV1
o Reduce the duration of hospitalization
Patients managed at home have increased
breathlessness w/c interferes with daily activities
and all those admitted to hospital should be
treated.
Prednisolone 30 mg every morning given for 7-
14 days.
Other treatment
IV aminophylline
If there is an inadequate response to
bronchodilators
LD and MD should be carefully chosen.
Oxygen therapy
Improve hypoxia
Predisposition to carbon dioxide
retention will be present.
Administration of high concentration of
oxygen can lead to an increase retention
of carbon dioxide and respiratory
acidosis.
Due to loss of hypoxic ventilator
drive
Mismatch between ventilation
and perfusion.
The goal is an initial oxygen saturation of
between 88% and 92% to avoid
respiratory acidosis but to allow enough
oxygen to be administered to overcome
potentially life-threatening hypoxia.
The initial concentration should be 24-
28% and then titrated to oxygen
saturation.
Arterial blood gases should be
monitored.
IV hydration
During an acute attack, pyrexia,
hyperventilation, and excessive work of
breathing can result in an inability to eat
or drink leading to dehydration.
Chest physiotherapy
Mobilized secretions
Promote expectoration
Expand collapsed lung segments
Nebuliser 0.9% NaCl has been also
used to help.
Doxapram
Largely superseded by non-invasive
ventilator support.
As a continuous infusion at a rate of 1-4
mg/min
For patients with
Acute respiratory failure
Carbon dioxide retention
Depressed ventilation
Uses:
Stimulates respiratory and
vasomotor centres in the medulla
Increases the depth of breathing
Slightly increase the rate of
breathing
Arterial oxygenation is usually not
improved because of the increased work
of breathing induced by doxapram.
Has narrow therapeutic index
Side effects:
Arrhythmias
Vasoconstriction
Dizziness
Convulsions
 Harmful if used when the PaCO2 is
normal or low.
Treatment of hypoxaemic and cor pulmonale
Cor pulmonale- if the resting PaO2 drops below
8 kPa
Treatment is symptomatic and involves managing
the underlying airways obstruction, hypoxaemic
and pulmonary edema that develops
Peripheral edema
o Thiazide or loop diuretics (reducing
respiratory drive)
Hypoxemia
o Oxygen- promote diuresis
All patient should be assessed for the need for
LTOT.
Domiciliary oxygen therapy
Aim: improve oxygen delivery to the cells
Increase alveolar oxygen tension
Decrease the work of breathing
to maintain a given PaO2
Can be given in 2 ways:
1. Intermittent (short burst)
administration
Increase mobility and capacity for
exercise and to ease discomfort
Most benefit in patient with
emphysema
2. Continuous LTOT
LTOT for atleast 15h/day-
improve survival in patients
with severe, irreversible
airflow obstruction,
hypoxemia and peripheral
edema
Box 26.5
The main aim of treatment is to achieve a
PaO2 of atleast 8 kPa without causing a
rise in PaCO2 of more than 1kPa
o Achieve by adjusting the oxygen
flow rate
Oxygen can be prescribed as oxygen
cylinders but 15h/day at 2L/min requires
1340L cylinders a week.
Use a concentrator w/c converts ambient
air to 90% oxygen using a molecular
sieve.
Tubing from the terminals delivers
oxygen to the patient, who wears a mask
or uses the more convenient nasal
prongs.
o Should be long enough to allow
some mobility.
PATIENT CARE
Pulmonary rehabilitation
Read the book
Stopping smoking
Once a decision to quit has been made, it is the
degree of dependence rather than the level of
motivation that will influence the success rate.
NRT, bupropion, varenicline
Nicotine replacement
Table 26.5
Stimulation of nicotine receptors in the brain
and subsequent release of dopamine.
o Leads to reduction in nicotine
withdrawal symptoms.
Act as coping mechanism, making cigarette
smoking less rewarding.
Doubles smoking cessation rates compared
with controls (either placebo or no NRT),
irrespective of the intensity of adjunctive
therapy.
The strongest evidence is for the use of
patches and gum.
The choice of product and initial dose is also
influence by the degree of tobacco
dependence.
Heavy smokers (15 to 20+ cigarettes a day or
smoking within 30 min of waking) requires
higher NRT doses.
Long acting
Long acting transdermal patches- most
suitable for people who smoke regularly.
24h-patch, worn overnight- better for
people who crave nicotine first thing in
the morning.
o Can cause insomnia or vivid
dreams
o Removed before bedtime or a
16h-patch used instead.
Heavy smokers should be started on the
high dose patches
Short acting
Gum
It is important to chew nicotine
gum correctly.
The gum should be chewed
slowly until the taste becomes
strong and then allowed to rest
between the cheek and teeth to
allow absorption.
Nicotine gum is not a good choice
for people with dentures or other
vulnerable dental work.
Encouraged to use 10-15 pieces
of gum a day. (one piece an hour)
Lozenge
Dissolve in the mouth and
periodically moved around, until
completely gone.
One lozenge per hour is
recommended during the initial
period of use to provide
adequate nicotine absorption.
Inhalator
Useful for people who miss the
physical act of smoking.
Nicotine is absorbed via the
buccal mucosa, peaking in 20-30
min.
User should puff on the inhalator
for 2 min each hour, changing the
cartridge after three 20 min
session.
Nasal spray
Useful for people who smoke 20
or more cigarettes per day.
SE:
Sneezing
Burning sensation in the
nose
The SE usually wears off after a
day or two.
Sublingual tablets
Dissolve under the tongue
Useful for people with denatures
who have difficulty using nicotine
gum.
Hourly use should be
recommended.
Bupropion
Antidepressant
Use in smoking cessation
Inhibits neuronal noradrenaline and
dopamine uptake
Reducing tobacco withdrawal
symptoms by increasing CNS
dopamine levels.
Treatment should be started while the
patient is still smoking with a target date to
stop smoking set during 2nd week of use.
Total treatment period- 7-9 weeks
Initial dose: 150 mg daily for 6 days,
increasing to 150 mg twice a day thereafter
(with atleast 8 hours between doses)
As effective as NRT and intensive behavioral
support.
Better result if used in combination with NRT
Not be used in patient with a current or
previous seizure disorder or in patients with
Bulimia
Anorexia
Bipolar disorder
Severe hepatic cirrhosis
Or those taking MAOIs
Inhibits CYP450 enzymes = inhibit
metabolism of other drugs
SE:
Dryness
Insomnia (avoid bedtime dosing)
 Headache
Dizziness
Allergic reactions
Taste disorder
Seizure
Varenicline
Oral selective partial 4 B2 agonist at the
neuronal nicotinic acetylcholine receptor.
Alleviates the symptom of craving and
withdrawal, whilst reducing the rewarding
and reinforcing effect of smoking by
preventing nicotine binding to 4 B2
receptors.
Result higher abstinence rate
Not be sustained after 12 months.
Recommended as an option for smokers for
smokers aged 18 or over wishing to quit.
Should be started 1-2 weeks before stopping
smoking.
SE:
N&V
Abnormal dreams
Insomnia
Increased risk of depression and suicide
Individuals who develop agitation, depressed
mood or suicidal thoughts are required to
seek medical advice.
Combination therapy involving varenicline
and bupropion (either with each other or in
conjunction with NRT) is not recommended.
Dominiciliary oxygen therapy
15 hr treatment of the day.
If an oxygen concentrator is used, limited
mobility can be gained by installing atleast 2
terminals for the unit with long tubing between
the terminal and nasal prongs.
Theres a fire risk if they used LTOT while
smoking.
Carbon monoxide present in tobacco smoking
binds to Hgb and forms carboxyhemoglobin, w/c
decreases the amount of oxygen that can be
transported by the blood and will partially or
completely negate the beneficial effects of LTOT.
The long term, chronic nature of COPD may leave
a patient with a fear of exercise as this will cause
dyspnea (breathlessness).
Ambulatory oxygen cylinders can be used to
encourage mobility and increase exercise
tolerance during travel outside the home.

Use of inhaled therapy

For individuals suffering from obstructive
airways disease with a degree or reversibility
Correct use of inhaled therapy is a vital part
of overall management.
More rapid onset of the B2 agonist to relieve
breathlessness
Regular administration must be stressed.
Incorrect use may lead to subtherapeutic
dosing.