This document defines COPD and discusses its pathogenesis, risk factors, clinical presentation, investigations, management, and acute exacerbations. COPD is characterized by progressive, partially reversible airflow obstruction caused by noxious particles like cigarette smoke. It is associated with systemic manifestations and comorbidities that worsen its severity. Spirometry is key to diagnosis and severity assessment, showing reduced FEV1 and FEV1/FVC ratio. Management involves smoking cessation, pharmacotherapy including bronchodilators and inhaled corticosteroids, oxygen therapy, and pulmonary rehabilitation. Acute exacerbations are acute worsening of symptoms and may require hospitalization for treatment with systemic corticosteroids and antibiotics.

1. Chronic Obstructive Pulmonary Disease
*Refer CPG of COPD/Kumar pg 835
Definition  preventable andtreatable respiratorydisorder largelycaused by smoking, is characterisedbyprogressive, partially
reversible airflow obstruction andlung hyperinflationwith significant extrapulmonary(systemic)manifestations and
comorbidconditions maycontribute to the severityof the disease in individual patients.
 The co-morbidconditions include:(increaseseverityof dz)
a) ischaemic heart disease;
b) hypertension;
c) osteopenia, osteoporosis andbone fractures;
d) cachexia andmalnutrition;
e) normochromic normocytic anaemia;
f) skeletalmusclewasting andperipheralmuscle dysfunction;
g) diabetes mellitus;
h) sleep disorders;
i) cataracts andglaucoma;
j) lung cancer;
k) anxietyand depression both
 The chronic airflow limitation - due to a mixture of smallairwaydisease (obstructive bronchiolitis) andlung parenchymal
destruction(emphysema)
 Airflowlimitation, associatedwithanabnormal inflammatoryreactionof the lungto noxious particlesor gases, the most
common is cigarette smoke, is usuallyprogressive, especiallyifexposure to the noxious agents persists.
Epidemiology  The prevalence ofmoderate to severe COPD in adults aged 30 years or above in the Asia-Pacific regionwas estimatedto
be at approximately6.3% andfor Malaysia at 4.55%.
 Mortalityand morbidityratesinthe Asia-Pacific region - higher inmen and increasedwith increasing age
Risk Factor Risk Factor Mechanism
Gene Severe alpha-1 antitrypsin enzyme deficiency causes panlobular emphysema inbothsmokers and
non-smokers (young age).
 Most commonlyseeninNorthern European
 Alpha-1 Antitrypsin(AAT) – produce byliver, proteinase inhibitor- inhibit neutrophil elastase
(inhibit elastinin alveolar wall and degrade elasticityof lung), secreted into blood and diffuse
into lung
 3 mainphenotype: MM(normal), MZ (heterozygous), ZZ (homozygous deficiency)
 Normallypt have liver cirrhosis, mayassociatedwithpancreatitis/IBD andetc
Exposure to
particles
A. Tobacco smoke - most common;lessthan10 pack years is uncommon (1 pack year = 20
cigarettes/day/year)
 Smoke particles inthe lungs leads to aninflammatoryresponse,increasedmacrophage
and neutrophilinfiltration into the lungs. These immune cells release cytokines,
chemokinesand elastases - degrade elastin, destruction ofalveolar andcapillary.
B. Organic dust and chemical-Ammonia, hydrogen sulphide, inorganic dust and organic dust
(livestockfarmer)
C. Indoor air pollution(heating and cooking)- biomassand coal
D. Outdoor air pollution- motor vehichles
Lung growth and
development
Anyfactor affects lung growth during gestationandchildhood has potential for increasing risk.
Oxidative stress Results fromanimbalance betweenoxidants (generated byphagocytes during mitochondrial
electron transport, air pollutants, cigarette smoke, etc.) andantioxidants, directlyinjures the lungs
and initiates lung inflammation
Gender Women are more susceptible to the effects oftobaccosmoke thanmen
Infection
Chronic IV drug
user/
socioeconomic
status
IV drug users ofcocaine, methadone and heroinare at higher risk;this is attributedto the vascular
damage induced bythe insoluble filler (cornstarch, cellulose, talc, fiber etc)

2. Pathology/
Pathogenesis
 Increase in the numbers of neutrophils(in the airwaylumen), macrophages(inthe airwaylumen, airwaywall, and
parenchyma), andCD8+ lymphocytes (inthe airwaywall andparenchyma)
 Emphysema: The inflammatoryresponse, mediatedbyneutrophils, macrophagesand CD8+ T-cells, release inflammatory
mediators and enzymes that damage the lungparenchyma. Proteaseslike elastase andmatrix metalloproteinases (MMPs)
released bythese inflammatorycells break downthe connective tissue of the alveolar walls andthe septae. A lossof
elastic recoil leads to diminished expiratoryflowrates, air trappingandairwaycollapsing.
 Chronic bronchitis: Mucous glandenlargement, goblet cellhyperplasiaandmucociliary dysfunctionoccur in larger airways,
causing excessive mucus productionandbuild-upreducingthe airwaylumen. Althoughthese pathological changes inthe
large airways, it appears that the major site of increasedairwayresistance is the small airways (≤
2mm). Fibrosis andsmoothmuscle hypertrophy mayoccur alongwith excess mucus production andcellular infiltration in
the peripheral airways.
Pathophysiolog
y
Emphysema Chronic Bronchitis
Parenchymal destruction: Recurrent damage to the alveoli
eventuallyleads to septal destructionalongwith the
capillarybedalso.
Matched V/Q (ventilation/perfusion ratio) defect: Since
both the terminal bronchioles andalveolialong withthe
capillarybedhave been destroyed, areas oflow ventilation
also have poor perfusion.
Mild hypoxia: Hyperventilation develops andcardiac
output (CO) drops whichleads to areasof poor blood flow
in relativelywell oxygenatedareas. Due to thispoor CO,
the rest of the bodysuffers fromtissue hypoxia.
Cachexia: At the pulmonarylevel, the low CO leads to
pulmonarycachexia;which induces weight loss andmuscle
wasting. This gives these patients the characteristic “pink-
puffer” appearance.
Small airway inflammation: Mechanisms discussedabove
lead to inflammationinthe smaller bronchioles andmucus
secretions further narrowthe airwaylumen. Despite this, the
parenchyma are relativelyless damaged.
V/Q mismatch: The physiologic response leads to a dropin
ventilationandcompensation withthe rise inCO. Increased
perfusion inthe areasof poor ventilationtakes place
eventuallycausing hypoxia andsecondarypolycythemia.
Severe hypoxia and hypercarbia: Chronic V/Q mismatch
leads to decreased oxygenation/deoxygenationof the blood
resulting inhypoxemia andincreased CO2 retention
(respiratoryacidosis ensues).
Pulmonary hypertension and cor pulmonale: Chronic
hypercapnia andrespiratoryacidosis leadto arterial
vasoconstrictioninthe lungs. With the retrograde pressure
build-up, the right ventricular pressures continue to rise and
eventuallycausing RV failure. Otherwise, knownas cor
pulmonale.

3. History clerking  Dyspnoea (hallmark)
 Progressive over months or years and is persistent. As lung functiondeteriorates, the breathlessness interferes with
patients’ dailyactivities.
 Cough
 Initiallyintermittent but later present daily, oftenwithchronic sputum production
 Extrapulmonarymanifestation and comorbidities
 Wheezinng and chest tightness
 Exposure to risk factor
i) Smoking history:
 Quantificationof tobaccoconsumption:total pack-years = (number of cigarettes smoked per day÷ 20) x
number of years of smoking
ii) Occupationalandenvironmental exposures to other lung irritants
 Impact ofdisease on psychosocial well being
 PMH- Exacerbationandadmissionfor resp illness
 FHx of resp dz
 Presence of comorbidities
 Current medicaltherapyandits appopriateness
 Social andfamilysupport available for pt
Physical
Examination
A. General Examination
 Tachypnoea
 Long term O2 therapy
 Hand- Warmpalm, finger clubbing, nicotine stained finger, asterixis (flapping tremor) ,boundingradialpulse
 Neck- Increase JVP(cor pulmonale), Use acessorymusclesof breathing
 Face- central cyanosis (nasolabial), polycythemia (like red eyes), pursed lip
B. Respiratory(chest)Examination
a) Inspection
 Barrel chest (anterior posterior diameter increase- seen inchronic hyperinflation:asthma, COPD)
 Scars (previous surgicaland chest drains)
 Others- dilatedveins, skindiscoloration, visible pulsation, radiotherapyskin changes(erythema andskin
thickening)
b) Palpation
 Chest expansion
 lung shouldexpandsymmetricallybyat least 5 cm
DLCO (diffusing capacity of
lung): extentto which
oxygen passes from theair
sacs ofthelungs into the
blood

4.  Reduce expansion side= lesionside
 Unilateral/ bilateral (chronic airflow limitation- bilateral)
 Apex beat
 Vocal fremitus-repeat “nenek-nenek”, compare bothside-upper, middle, lower (increase= consolidationfibrosis
and above pleural effusion;decrease= pleural effusionor collapse)
c) Percussion-hyperresonance
d) Auscultation- ronchi (airwayobstruction,CA, cardiac failure), loudS2 (pulmonaryHTN), prolongedexpiration,
reducedbreathsound)
C. Loss ofcardiac andliver dullness
D. Leg- ankle edema (cor pulmonale)
Investigation 1. Lung fx test (spirometry/ peakflow meter)
 Spirometryis performed inpeople withexposure to risk factors whohave chronic coughand sputum productioneven
without dyspnoea as it mayhelpidentifypatients earlier inthe course of the disease
 Criteria to interpret
FEV1  Volume expiredinthe first secondof a forcedmaximal expiration
 Initiatedafter maximalinspiration;measure ofhowquicklyfulllungs empty
FVC Maximumvolume ofair whichcanbe expired withmaximal force (after a maximal inspiration)duringa forced
manoeuvre
FEV1/FVC
Or FER
Show index of airflowlimitation
PEF Maximal expiratoryflow rate achievedduring the forcedexpiratorymanoeuvre (L/s)

5.  Use the FEV1 /FVCratioto detect obstruction – Use FEV1 as % predictedto grade severityof obstruction
 Use FVC(or VC) to assess restriction – Low FVC(VC) inpresence ofsignificant obstruction does not
necessarilyindicate restriction – Need to confirmandquantifyrestriction withmeasurement of TLC
 Peak flowmeasurements detect airflow limitation but has poor specificity. The relationshipbetweenpeak expiratory
flow andFEV1 is poor inCOPD
2. Bronchodlator reversibilitytest
 Response to a bronchodilator is considered significant ifthe change inFEV1 is both at least 200 mL and 12% above
the pre-bronchodilator FEV1
3. CXR: presence ofhyperinflation(flatteneddiaphragmandincreasedlung volume), bullae andhyperlucencyof the lungs
4. ABG:performedinpatients withFEV1 < 40% predictedif theyhave lowarterial oxygen saturation (less than92% on pulse
oximetry) or with clinical signs ofrespiratoryfailure or cor pulmonale as these patients maybenefit fromlong term oxygen
therapyat home
5. FBC:anemia ofchronic dz/polycythemia for chronic hypoxaemia
6. ECG: pulmonaryHTN
7. Alpha-1 Antitrypsindefeciencyscreening:performed inyoungCOPD patients (< 45 years old) or those whohave a strong
familyhistoryof the disease.
8. 6 Minutes WalkTest
 Measures the distance coveredduring six minutes
 Arterial oxygendesaturationcanbe measured witha pulse oximeter duringwalking.
9. Others: to detect other commonco-morbidities
 fasting plasma glucose
 serum albumin

6.  serum fastinglipids
Differential dx
(Mnemonic:
ABCDVT)
a) Asthma
b) Bronchoectasis
c) Congestive Heart Failure
d) Diffuse parenchymal lungdz
e) PulmonaryVascular dz
f) Tuberculosis
Severity
Follow up Evaluationof the following:
 Exposure to riskfactor:askabt smokingandwillingnessto stop
 Current sx andnew or worseningsx;consider comorbidities
 P/E and checkfor:
a) BMI, weight-nutritional status
b) Respiratoryfailure/ cor pulmonale
c) Anyconcomittant dz
 Spirometrymeasurement
 Medication effectivenessand compliance (MDI correct use?)
 Exacerbation hx:
 Causes, frequencyandseverityof exacerbation
 Increase needof bronchodilator and systemic glucocorticoid- access severity
 Hospitalization shouldbe documented(duration, invasive + non-invasive ventilation)
 Pt education

7. Management
Pharmacotherapy
 Short Acting
1) Short Acting B2 Agonists – MDI salbutamol 200mcg, Fenoterol 200mcg ,
Terbutaline 500mcg PRN
2) Short acting Anti Cholinergics – MDI Ipratropium Bromide 40mcg QID
 Long Acting
1) LABA – MDI Salmeterol 50mcg BD, Formoterol 9mcg BD
2) LAAC – Tiotropium 18mcg OD
 InhaledCorticosteroids (ICS)
1) MDI Budesonide 400mcg BD
2) MDI Fluticasone 500mcg BD
 Combinations
a) MDI Combivent = Salbutamol + IpratropiumBromide (SABA + SAAC)
b) MDI Seretide = fluticasone propionate/salmeterol (ICS + LABA)
 Methyxanthines– Theophylline 125-300mg BD
 Corticosteroids
1) IV hydrocortisone 100mg QID1/7
2) T Prednisolone 30mg OD 5/7
LTOT (long term oxygentherapy)
 Indications
1) PaO2 <55mmHg or Sa O2
<88%, with/without
hypercapnia
2) Pa O2 55-60mmHg, SaO2
89% + pulm hpt, peripheral
edema (CHF), polycythemia
Surgical intervention
1) Lung volume reductionsurgery
2) Bullectomy
3) Lung transplantation

9. Acute exacerbation of COPD
Definition Natural course of the disease characterisedbya sustained (lasting 48 hours or more) worsening ofthe patient’s baseline
dyspnoea, cough, and/or sputum that is beyondnormal day-to-dayvariations, is acute in onset, and maywarrant a change in
regular medication
Causes a) Cigarette smoking
b) Bacterial/viralinfection
 Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydophila
pneumoniae, Klebsiellapneumoniae, Pseudomonas aeruginosa, Acinetobacter baumannii andStaphylococcus aureus
c) Enviromentalfactor
d) Unknownetiology
e) Other precipitating factors include congestive heart failure, coldair andpulmonaryembolism
Clinical
features
 Dyspnoea, cough and productionof sputum, confusion, lethargy
 Physical exam
1) Vital signs – T, RR, PR, BP
2) Poor prognosis – confusion, reducedconscious level, cachexia, respirator distress, cyanosis
3) Co morbids – CVS, DM, lung CA, neurovascular dz
Investigation 1) ABG
2) Sputum C&S
3) CXR
4) ECG
5) FBC, LFT, RP
Differential
DX
(ABCDEFP)
 Asthma (mayco-exist withCOPD)
 Bronchiectasis
 Lung cancer
 Diffuse parenchymal lungdisease
 Pulmonaryembolism
 Heart failure.
 Pneumothorax
Managemen
t