3 Copd

7/29/2019 3 Copd

1/17Internal Medicine | Chronic Obstructive Pulmonary Disease & Obstructive Sleep Apnea 1

COPD

COPD is primarily a disease caused by smoking with more than 90% of COPD patients

worldwide having the disease due to smoking. Smoking related deaths are huge with about5.4

millions/year, one every 6 seconds. Smokers on average have 10-15 years less survival rate

than their nonsmoking peers. In this lecture we will cover the following basics about COPD

briefly:

Definitions

Epidemiology

Risk factors

Pathology

Diagnosis

Treatment

Definition

It is defined as A disease state characterized by airflow limitation that is not fully reversible

and usually it is progressive and associated with abnormal inflammatory response of the

lungs to noxious particles or gases. It is a preventable and treatable disease.

From its name COPD Chronic obstructive pulmonary disease so it is a disease characterized by

airflow limitationor obstruction that is not reversibleand this is to differentiate it from

asthma as it is a reversible and normal lung function is attained once asthma is treated

adequately and this accounts for majority of asthmatics however COPD patients especiallythose with severe or moderately severe disease, whatever treatment they undergo their

condition will not reverse and go back to normal therefore it isnt entirely reversible.

It is a progressive diseaseas in as long as the patient is smoking the underlying inflammatory

changes will worsen as well as the airflow obstruction even if he/she is under medication.

It is a preventable and treatable diseaseas when and if we stop smoking there would be an

elimination of 90% of the COPD cases leaving it treatable but not curable as the treatment will

only ameliorate the symptoms but not reverse the disease or cure it.

7/29/2019 3 Copd

2/17

Internal Medicine | Chronic Obstructive Pulmonary Disease & Obstructive Sleep Apnea 2

Chronic Bronchitis & Emphysema

COPD is generally composed of two diseases chronic bronchitis and emphysema both of which

are smoke related and majority of patient have elements of both.

Chronic bronchitis is defined clinically by the presence ofcough and sputum for most of the

days in a period of at least 3 months on the course of2 consecutive years. This does not meanthat the patient will only cough for 3 months out of the entire year so if you do calculate the

number of days in which he is coughing and producing sputum in a year and theyre in total

about 3 months and this result is consecutive for 2 years without an underlying lung disease

such as TB they.

Emphysema is apermanent airspaceenlargementbeyond the terminal bronchioles with

destruction of alveolar septa. So if you observe the bronchial tree diagram as you can see the

trachea keeps dividing in a dichotomous way each one giving rise to two branches until the16

thand 17

thgeneration and this is where the site of chronic bronchitis is as well so it is a

disease of the conducting airways where is the emphysema effects the part involved with gas

exchange which is composed of the respiratory bronchioles, the alveolar ducts and the

alveolar sacs. So emphysema is a smoke related disease and causes emphysema in the central

part of the respiratory unit.

7/29/2019 3 Copd

3/17


Asthma VS. COPD

This is a comparison between asthma and COPD where asthma is usually cause by a

synthesizing agentand allergens whether its house dust mites, grass pollen or tree

pollen while COPD is a Noxious agentwhich is mainly caused by smoke/smoking.

The asthmatic airway inflammation is usually driven by CD4+

T lymphocytes and

eosinophils. So if you take a biopsy of an asthmatic airway you will find these three

components. In COPD however youll find CD8+ T lymphocytes, macrophages and

neutrophils. Asthma is usually completely reversible while COPD is irreversible.

COPD in USA

COPD is a major heath issue; nowadays in the states it is the 3rd

commonest cause of death

(11.8million). Until 2001 it was the 4th

with more deaths in females than in males. The majority

of COPD patients are undiagnosed (14million) and even with the underdiagnosed in 2005 theywere 126,000 deaths were recorded. Until recent records there are still a higher number of

females smoking in the states than males leaving their COPD cases higher.

7/29/2019 3 Copd

4/17


In 2010 was and for the first time a recorded of the prevalence of smoking going below 20%.

To the right is a graph of the six most

common causes of death in the US with

the COPD being the only one increasing

steadily since 1970 leaving others such as

cancer and heart diseases leveling or

decreasing.

7/29/2019 3 Copd

5/17


This is a comparison of the prevalence by gender as seen in the legend the red columns are

females and the yellow males. As you can see with every record the females are catching up

with the males and nowadays they are exceeding the number of deaths by smoking; The

reason being females start smoking later than females as men start in the 50s and 60s while

females from the 70s and above and the more you smoke the more likely you are to have a

COPD.

Risk factors of COPD

Regarding the risk factors; all chronic illnesses have a genetic elementand an

environmental factor. The only significant genetic disease is the -1 antitrypsin

deficiencywhich causes emphysema and is a very rare disease probably less than 1% of

all COPD cases.

Airway hyper-responsiveness patients are more likely to develop a COPD and it is amust in asthma patients which means that those who have their airways constricting to

common aeroallergens that did not answer to specific stimulants like metacholine or

histamine; if their airways do constrict they might have the airway hype-responsiveness

Lung growth; those who have prematurity or severe infections as infants and if they

smoke when they grow up, their COPD will be more severe than others.

As for the exposure factor the only significant one is the tobacco smoke as about 90% of

the COPD patients are affected due to it but the other factors that do affect smoking

7/29/2019 3 Copd

6/17


include infections, occupational dusts and chemicals, indoor and outdoor air pollution

and socioeconomical status as patient with higher socioeconomical statues have a

smaller chance of acquiring a COPD disease. Some researchers believe its due to rich

people being more exposed to antioxidants from fresh fruit and vegetables that

economically challenged people have less access to needless to say there is no such

thing as safe smoking i.e. even if the diet is sound smoking is still dangerous.

Prevalence of smoking in Jordan

The prevalence of smoking in Jordan is quite alarming. As we mentioned earlier in most

western countries the prevalence of smoking in decreasing except in the 3rd

world

countries. In 2007 patients above 18 years of age about 50% of them are smoking with

females being 10.5% which is indeed an underestimate of the female prevalence.

As for school children in 1999 children between 13 and 15 who experimented with

smoking (not regular smokers), and this is the way smoking starts as a habit throughexperimenting with it, males were 25% with females at 16% and in 2007 males worse to

37% and females 26%.

So as you can see with these numbers the prevalence of smoking in Jordan is alarmingand we expect more COPD and other smoke related diseases such as cerebrovascular

accidents, coronary vascular diseases and not forgetting lung cancer

Pathology and Pathogenesis

As you know smoke contains probably more than 400 substances most of which are harmful

causing inflammatory changes most of which are carcinogenicand due to all these

components in smoke. It causes hypertrophy in mucus secreting glands of the airways leading

to mucus hyper-secretion. It also impairs the function of the cilia and these two components

ciliary dysfunction and increased mucus secretion leads to chronic chough and sputum

production.

Airflow limitation is another complication due to inflammation and patients with emphysema

have hyperinflation of the lungs that leads to shortness of breath. And of course emphysema

affects the gas exchange unit that leads to hypoxia and chronic hypoxia which can lead to

right sided failure andpulmonary hypertension.

7/29/2019 3 Copd

7/17


In this image we have a small airway of a patient who is a smoker but does not have COPD. Do

note that not all smokers develop COPDit is for further reasons due to genetic

predisposition only 20-30% of smokers develop COPD. But if they do escape COPD they might

develop coronary heart disease, lung cancer or a stroke. Now back to the image;

a. Here you can see a relatively normal airway in a smoker who doesnt have COPDb. Here there is a case ofmild COPD and in the airway you can see the mucus with an

inflammatory change

c. Here the disease progresses and you can see more inflammatory changes

d. Here is the severe form where you can seeperi-bronchial fibrosis where around the

airways there is a band of fibrotic tissue and that is why the airways obstruction is

irreversible even if you provide him with bronchodilators.

As a comparison in asthma we dont see this peri-bronchial fibrosis we have some

mucosal collagen deposition which did not interfere much with the dilatation of the

airways after giving bronchodilators

7/29/2019 3 Copd

8/17


This is an image of the emphysema. You can see the terminal bronchiole, respiratory

bronchiole where you can see a dilatation known as the central lobular emphysema (CLE)

which is specific for smoke related emphysema and usually affects the upper lobes of the

lungs while the -1 antitrypsin deficiency causes pan-acinar which causes the entire acinus to

be dilated which usually also affects the lower lobes of the lungs more than the upper lobes.

So finally the airways inflammation

leads either

1. Small airways disease making the

airways smaller due to the

inflammatory and fibrotic changes and

mucus secretions and hypertrophy of

mucus glands which leads to airway

limitation2. Parenchymal destruction where even

with larger lungs the airways are

obstructed and the reason being that all

the airways are patented by the elastic

tissue in the alveolar wall

7/29/2019 3 Copd

9/17


Diagnosis and Clinical forms

As for the diagnosis of COPD as any clinical disease we need to consider the following:

Clinical features

Pulmonary function tests

Radiology

And we have confirmatory tests available to determine all three. The chief symptoms in

patients with COPD:

Chronic cough

Chronic sputum production

Dyspnea

History of exposure to risk factors

And alongside the symptoms is the patient has a risk factor included such as smoking then we

have to consider COPD and usually these patients are above 40+ because for a COPD to

develop due to smoking it needs to be done over a long period of time say 20 years + if the

patient is susceptible to COPD.

In general we have two clinical forms of COPD

a. Blue blotters: those who have predominantly chronic

bronchitis and not emphysema with chronic cough, sputum

production. These patients usually do into right-sided heart

failure and live with hypoxia hence the name blue blotters so

they are cyanosedbecause of the chronic respiratory failure and

they are blotted or edematous because of the heart failure that

led to the edema in the legs and congestion in the liver

b. Pink puffers: those who have predominant emphysemaand maintain their oxygenation with a pinkish color of the skin

and severe shortness of breath. If you receive two patients one

with pure emphysema and one with chronic bronchitis and they

have the same degree of airway obstruction the emphysema has

a worse prognosis. Once those with emphysema (pink puffers)

develop hypoxia or right-sided failure its usually the end of their

life.

BUT THE MAJORITY OF PATIENTS HAVE ELIMENTS OF BOTH a&b

7/29/2019 3 Copd

10/17


Pulmonary Function Tests

Once we consider the patient to having a COPD case we have to prove it by performing a

pulmonary function test. Just like when you suspect a patient to having diabetes from the

symptoms youd perform a blood sugar test.

The COPD test is known as the simple spirometery test. In it we have the first test value of

FEV1/FVCwith FEV1 being theforced expiratory volume in the first secondi.e. when you take

a deep breath and you blow out; in the first second normal people can expel up to 80% of thei

vital capacity because the amount of air that we can inhale in one breath is called theforced

vital capacityFEV.

Now patients with COPD they cannot expel that amount of air in the first second andusually their ratio is less than

7/29/2019 3 Copd

11/17


Classification of COPD Severity

The severity of COPD is classified according to the reduction rate of the FEV1 keeping in mind

that the ratio is always less than 80% predicted

As always the ratio is less than 0.7 but the FEV1is still above 80% so its within normal ranges

and if the patient stops smoking he would probably lead a normal life as the FEV1 is still

preserved.

Stage II: Moderate

o FEV1/FVC < 0.70

o 50% < FEV1 < 80% predicted

Stage III: Severeo FEV1/FVC < 0.70

o 30% < FEV1 < 50% predicted

Stage IV: V. Severe

o FEV1/FVC < 0.70

o FEV1 < 30% predicted or

o FEV1 < 50% predictedplus chronic respiratory failure

7/29/2019 3 Copd

12/17


Above you can see a comparison between a normal chest x-ray (left) and a patient with

emphysema (right). As you can the picture on the right where the lungs arehyper inflatedand

the diaphragm isflatinstead of being dome shaped. If you do suspect emphysema however,

the plain chest x-ray is not sensitive and therefore you need to perform a HRCT scan (High

Resolution Computed Tomography).

As you can see here the HRCTshows a lung with emphysema and

is characterized through the

presence of multiple

radiolucencies in the image and

affects the upper lobes of the lung.

To the right you can see another

HRCT but of emphysema caused

by the -1 antitrypsin which is

panacinarand it affects the

central part of the respiratory

unit.

7/29/2019 3 Copd

13/17


Sometimes emphysema join together

to form large bullae (the large black

bodies in the HRCT)

Treatment

Once we diagnose the COPD we start the treatment and the first aim of the treatment is to

halt/stop the disease progression and the only way to do that is to STOPSMOKING. So we

have to advice every patient that has COPD to stop smoking.

Now some patients can do it by themselves while other may need assistance which is provided

through nicotine replacement patches or some forms ofanti-depressants and of course the

nicotine receptor agonistVarenicline which have all proved to be of help although in spite of

all these given supports only about 20-30% of smokers do actually manage to quit smoking

completely.

But of course if we are able to get such an amount, 20-30%, to quit smoking it would be

immensely helpful.

Always ask the patients to stop smoking altogether as studies have proven that the successful

rate of patients who quit from day one is higherthan patient who quit on intervals or by

reducing the amount of cigarette consumption. This could be due to the patients contact with

the smoking source and the possibility of the patient compensating for the reduced mount

one way or another. The patient might have withdrawal symptoms as smoking fulfills the

7/29/2019 3 Copd

14/17


criteria of an addiction both physically and mentally in which case nicotine replacement prove

helpful.

If the reason for COPD is occupational then the patient is advised to change his/her occupation

and if the patient has -1 antitrypsin deficiency you can provide a replacement for the missing

-1 antitrypsin.

The second most important thing is to provide the patient with the right medical treatment

through bronchodilators, rehabilitations and in some patients they may need surgical

treatments.

As Ive mentioned before, 20-30% of smokers develop COPD normally after the age of 25 as

the maximum pulmonary function is attained at the age of 25. After the age of 25 we lose 20-

30ml of our FEV1 yearly. In smokers susceptible to COPD they lose 70-80ml of their FEV1 yearly

For example if a man of 25 years of age has an FEV1 of 3.5L and he reaches the age of 50

without smoking he would only lose about 1L (20ml * 50yrs) of his FEV1 and at age 75 his FEV1will be 2.5 and if you have an FEV1 you are actually able to tolerate pneumonectomy which is

removing one of your lungs and you can survive without having a respiratory failure.

However if the patient is a smoker and as a result loses 70ml of his FEV1 every year by the age

of 50 he would have lost 3.5L of his FEV1 which means he would die 10-15 years earlier than

that. So this is the reason we insist on smoker who are susceptible to COPD to stop smoking is

because by the age of 60 theyd die. It is never late to quit smoking as when you do you start

7/29/2019 3 Copd

15/17


only losing 20ml of your FEV1 again giving you more time each year but if you do have COPD

and continued to smoke the deterioration in lung function will continue. The drug treatment

will only improve your symptoms but it will not improve the pulmonary function.

This graph here shows a

comparison between

someone who continued to

smoke (bottom line) and

someone who stopped

smoking (top line). As you

can see the person who

stopped smoking will have

an improvement in hispulmonary function in the

first year and then will start

decreasing as a normal

persons rate of declining

FEV1 by losing 20ml instead

of 70ml every year.

Outpatient Management of COPD

Regarding the management for all the COPD patients whether they have a mild case or a

severe case we have to

Avoid risk factors: which is smoking and we have to administer the patients with

influenza vaccineevery winterand thepneumococcal vaccineonce in their lifetime

which would prevent infections.

In asymptomatic shortness of breath cases: we give them bronchodilators such as

salbutamolor ipratropium In symptomatic shortness of breath cases: we give them long acting bronchodilators

such as Formoterolor Salmeterol. We also give a long acting anticholinergic known asTiotropium which is given once daily

For a more severe disease with frequent exacerbations (attacks of increasing coughs+

sputum+ shortness of breath): we give inhaled corticosteroids as studies have shown

that they reduce the exacerbations in these patients as certain patients with COPD are

7/29/2019 3 Copd

16/17


more prone to exacerbations than others as some studies have shown that with the

same degree of airway obstruction some patients for some reason have a higher loss

rate of pulmonary function due to exacerbation more than others and long term

inhalation of corticosteroids have proven beneficial.

If they develop respiratory failure: we have to supplement them with O2 at home as

they require long term home O2 therapy.Surgical Treatment

Rarely do we have patients who may benefit from surgical interventions but they do include

Lung volume reduction

o It is performed on patients withpure smoke related emphysematherefore it isnt

a treatment for chronic bronchitis. This is conformed via a HRCT scan where the

upper lobes are shown to be predominantly destructed and the lower lobes a

mostly spared. They upper lobes are extracted giving more space to the relatively

normal lower lobes to improve their function.

Bullectomy

o In the presence oflarge bullae that compromises the relatively normal lung tissue

we extractit to improve the function of the lung for the patient

Lung transplantation

o although no one performs a lung transplant for a smoker as they may abuse the

new lung and smoke again

o candidates for a lung transplant include patients with -1 antitrypsin deficiency as

these patients develop the disease in their early 30 and if they are not given the

appropriate replacement of the substance they might go into respiratory failure

Acute Exacerbations

Patients with acute exacerbations usually have respiratory failure during the

exacerbation which means that their PO2 at less than

7/29/2019 3 Copd

17/17

azithromycin or clarithromycin. According to the severity of the exacerbation we might

give other antibiotics but we usually cover gram ve organisms like Haemophilus

moraxella and thepneumococcalwhich is gram +ve.

Corticosteroids are given during exacerbation as we give parenteral either intravenous

or oral if the patient does not have any GI problems such as vomiting. Usually we give

40-60mlof Prednisolone which is for the exacerbation period only i.e. 2-3 weeks only

as some studies have shown that some COPD patients under long periods will havehigher risks than benefits.

Assisted ventilation is given if the patient develops a respiratory failure with

unmaintained oxygenation. It could be noninvasive through aface maskor mechanical

ventilation through endotracheal tube

So generally with each exacerbation the quality of life of the patient will deteriorate and the

lung function will deteriorate therefore we have to do everything we can to prevent

recurrence of the exacerbations but giving treatments such as the long term bronchodilators ,inhaled corticosteroids and of course if the patient can he must quit smoking.

This graph here shows a study that

explains the benefit; the more you

use the long term oxygen treatment

for example the redline represents

exposure for 24hours which is

better than the black line which was

for 15hours. The minimum is

12hours a day that have shown

survival benefits. If you use it for

less than 12 hours it may show

symptomatic improvements but it

wont show any survival benefits.

Done by

Mohamed Harun Sanoh

Documents

3 Copd