COPD

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Ayşe Baha, MD
Near East University Faculty of Medicine
Chest Diseases

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 Definition
Reaction to harmful gases and particles.

It is a widespread, preventable, and partially treatable disease

associated with an increased chronic inflammatory response of the
airways and often characterized by progressive permanent airflow
restriction.

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Epidemiology
• It is the 3rd mortal disease in the world.

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Epidemiology
• Prevelance 5% to 20% (varies in different parts of the world).
• There are 8 billion people in the world, 65 million of them COPD
• But; It is assumed that 9 out of 10 patients cannot be diagnosed

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 RISK FACTORS

Genetic factors (Alfa 1 Antitripsin deficiency ) Problems during the growth and development
of the lungs (prematurity, maternal smoking,
childhood respiratory infections)
Tobacco smoke (MAIN) Gender (M>F)
Organic and inorganic occupational exposure Age (>40 years-old)
to dust and chemicals
Air pollution within the home Chronic Respiratory airways infection (BE)
(in particular the use of biomass fuels for Socioeconomic level
heating and cooking within a enclosed area.) Chronic bronchitis

Environmental air pollution Asthma

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 Components of COPD
1. Chronic Bronchitis 2. Emphysema

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Chronic Bronchitis

Productive cough of more than

3 months occurring within a
span of 2 years.

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Chronic Bronchitis: Clinical Characteristics
• Chronic bronchitis is characterized by
the excessive production of mucus with
productive cough
• Blockade of bronchioles by mucus,
inflammation and edema

• Presentation
• Smoking, Early onset (20-30 yrs)
morning productive cough
• Diagnosis usually occurs at 50-60 yrs
• Smoking is the most significant risk factor
• Repeated respiratory infections are common
• Productive cough, often purulent sputum, late onset dyspnea, early onset chronic cough
• Patient is typically obese
 Chronic Bronchitis: Pathophysiology
• Repeated irritation and inflammation
leads to bronchiolar smooth muscle
hypertrophy and reduction in airway
diameters
• Increase in size and number of
submucosal mucus glands and goblet
cells
• Goblet cells proliferate in bronchioli, which
normally do not contain mucus-secreting cells
• Mucus is thick and difficult to clear from airways
• Ciliary action is impaired by
inflammation, resulting in poor clearance
of mucus, leading to repeated bacterial
infections
Chronic Bronchitis: Pathophysiology

• Hypoventilation common
• Elevated blood CO2 and reduced O2, cyanosis
• Often termed “blue bloaters”
• Loss of respiratory drive unexplained
• Death results from right heart failure (cor
pulmonale) due to pulmonary hypertension, or
respiratory failure
 Emphysema
Emphysema is damage to the alveolar walls.
Develops over time and involves the gradual damage of lung tissue.

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 Emphysema: Clinical Characteristics

• Emphysema results from acinar distension and destruction of alveolar

membranes
• Loss of surface area for gas exchange
• Later onset than CB (30-40 yrs)
• Diagnosis usually occurs at 60-70 yrs
• Minimal history of cough
• Chief complaint is shortness of breath
• Patients typically hyperventilate to maintain normal blood gases
• “pink puffers”
• Environmental risk factors: smoking, dust inhalation, pollution
• Patients are typically thin, sometimes “barrel-chested”, pursed lip.
Comparing pink puffer and blue bloater

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 Normal inspiration is performed.
However, during expiration, the
airway closes before the alveoli (due
to airway fibrosis and muscle
contraction).

Air remains in the alveoli. Since

there is only air left for the alveoli,
the patient cannot breathe
sufficiently in the next inspiration.

If this continues, shortness of breath

develops.

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 Teaching
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The diagnosis must be confirmed by spirometric examination

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Dyspnea
• There are 2 evaluation method!
• mMRC (modified Medical Research Clouncil)
• CAT (COPD assessment test) (not only Dyspnea but also another symptoms)

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The patient scores each question

from 0 to 5.
(0; I am very happy)
(5; I am very sad)

There are 8 questions

Questions; cough, mucus, chest tight,

physical activity

Total point: 0-40.

<10 point: mild symptom
10 and >10 point: severe symptom

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PHYSICAL EXAMINATION

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DIAGNOSIS

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SPIROMETRY (Pulmonary function test: PFT)
GOLD STANDART METHOD FOR DIAGNOSIS OF COPD

• FVC: forced vital capacity

• FEV1: volume exhaled in 1 second
• FEV1 / FVC
• Spirometric measurements are compared with reference values ​determined
according to age, height, gender and race.

• A FEV1 / FVC <70% measured post bronchodilator indicates permanent airflow

limitation. (COPD)
• And FEV1 level shows us “obstruction level”

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Mild exacerbation: not

leading hospitalization

Moderate exacerbation:
not leading hospitalization
but need systemic steroid
and/or antibotic

Severe exacerbation:
leading hospitalization

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Assess and Monitor Disease
• Patient Group A- Low Risk, Less symptoms
• Gold 1 or 2 and/or 0-1 exacerbations per year and mMRc 0-1
• Patient Group B-Low Risk, More symptoms
• Gold 1 or 2 and/or 0-1 exacerbations per year and mMRc ≥2
• Patient Group E High Risk
• Gold 3 or 4 and/or ≥2 exacerbations per year and mMRc 0-2
 CHEST X-RAY
Not specific for diagnosis.
To exclude other diagnoses such as;
• Heart failure,
• Tuberculosis,
• Bronchiectasia,
• Lung cancer
It is important in evaluating the presence of additional diseases
and complications.
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CHEST X-RAY

COPD
• Aeration increase
• Flattening of the diaphragm
• ‘‘Tear drop’’ heart
• Deletion in
peripheral vascularization
Normal
• Widening of central
pulmonary arteries (in the presence of Pulmonary Hypertension)

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COPD DIFFERENTIAL DIAGNOSIS
• The most important disease in differential diagnosis is asthma.

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 The most important disease in differential diagnosis is asthma.
Other diseases to be considered in the differential diagnosis of COPD

Congestive heart failure

Bronchiectasis
Tuberculosis
Obliterative bronchiolitis
Diffuse panbronchiolitis

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PREVENTION OF COPD TREATMENT OF COPD
(most important to least important)

• Prevention and Cessation of smoking • Cessation of smoking

• Improving Inequality in Health • Prevention of Indoor and Outdoor Air

• Prevention of Indoor and Outdoor Air Pollution

Pollution • Prevention of Occupational Exposure

• Prevention of Occupational Exposure • Regular Physical Activity
• Regular Physical Activity • Vaccination

• Medical treatment

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TREATMENT of STABLE COPD

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LABA: Long Acting Beta Agonist

LAMA: Long Acting Antimuscarinic
ICS: Inhaler Cortico Steroid

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Pharmacological Treatment of Stable COPD

BRONCHODILATORS MAIN
TREATMENT
Anticholinergics (antimuscarinic), Beta 2 agonists, Methylxanthines OPTION

CORTICOSTEROIDS
Systemic corticosteroids, Inhaled corticosteroids

PHOSPHODYESTERASE-4 INHIBITORS ANTI-

Roflimulast INFLAMMATORY
TREATMENT
OPTIONS
OTHER MEDICINES
Mucolytics

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SABA, SAMA LABA, LAMA

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BRONCHODILATORS

▪ MAIN treatment of symptoms control.

▪ Inhalation therapy is preferred.

▪ Combining bronchodilators increases the effectiveness of treatment.

▪ Short acting bronchodilators:

▪ SABA (Short Acting B2 Agonist), SAMA (Short Acting Muscarin Antagonist)

▪ Long acting bronchodilators:

▪ LABA (Long Acting B2 Agonist), LAMA (Long Acting Muscarin Antagonist)

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BRONCHODILATORS - BETA 2 AGONISTS
• Beta-agonists are also called “beta-adrenergic agents.”
• SABA (Short Acting B2 Agonist)
• Typically used as "rescue" medications to provide quick relieve of symptoms.
(used as need!!)
• Onset of action of under 5 minutes and a therapeutic effect duration between 3
to 6 hours.
• LABA (Long Acting B2 Agonist)
• Typically used as "main" medications to provide long term relieve of
symptoms. (used regularly)
• LABA's have onset of duration greater than 5 minutes compared to the SABAs,
with up to 15 minutes for salmeterol and a duration of effect of at least 12
hours.

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 BRONCHODILATORS - BETA 2 AGONISTS
β2 Agonist Mechanisms of Action B2-agonists relax airway smooth
muscle by stimulating beta2-
adrenergic receptors.
It increases cyclic AMP and
antagonizes mechanisms of
bronchoconstriction.

β2 agonists open large

conductance calcium-activated
potassium channels and thereby
tend to hyperpolarize airway
smooth muscle cells.

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 BRONCHODILATORS - BETA 2 AGONISTS
B2 Agonist Molecules Side effects
• SABA • Hypertension
• Salbutamol • Tachycardia
• Terbutalin
• Fenoterol • Palpitations
• Levalbuterol • Restlessness
• LABA • Tremors
• Formoterol • Dizziness
• Salmoterol
• Indacaterol • Urinary retention
• Olodeterol • Nausea, vomiting
• Arformoterol

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BRONCHODILATORS – ANTIMUSCARINIC (anticolinergic)

It causes relaxation in bronchioles by blocking muscarinic receptors in

bronchiolar smooth muscle cells (parasympathetic (acetic choline) receptor
antagonists).

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BRONCHODILATORS – ANTIMUSCARINIC (anticolinergic)

Antimuscarinic molecules Side effects

• SAMA
• Ipratropium (mostly using)
• Oxitropium
• LAMA
• Tiotropium (mostly using)
• Glycopyronium
• Aclidinium
• Umeclidinium
• Revefenacin

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BRONCHODILATORS-Theophylline (methylxantine)
• It is indicated as the last choice in the treatment recommendation scheme.
• Theophylline can be used in cases where it is not possible to access drugs, in
patients who do not have access to social services and cannot take inhaler drugs.
• However, side effects should be closely monitored.

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Theophylline Mechanism of Action

• Nonselective Phosphodiesterase inhibitor

• Must be the last choice due to side effects and narrow therapeutic range
• Theophylline blood level should be monitored in patients who are started treatment
(12-20 mcg).
• Below this level, no bronchodilation effect is observed, but an anti-inflammatory effect
can be observed.
• Increases mucociliary clearance
• Increases diaphragm contraction power
• Has a diuretic effect
• Positive inotrope, positive chronotrope
• Anti-inflammatory effect
• Mild bronchodilator effect

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 Theophylline Side Effects

CENTRAL NERVOUS SYSTEM

Headache,
CARDIOVASCULAR SYSTEM
Insomnia
Atrial arrhythmia Irritation
Ventricular arrhythmia Convulsion

DRUG INTERACTION
GASTROINTESTINAL SYSTEM Cimetidine
Anorexia Nausea Rifampicin
Vomiting Erythromycin
Gastroesophageal reflux Quinolones etc
.

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Pharmacological Treatment of Stable COPD

BRONCHODILATORS MAIN
TREATMENT
Anticholinergics (antimuscarinic), Beta 2 agonists, Methylxanthines OPTION

CORTICOSTEROIDS
Systemic corticosteroids, Inhaled corticosteroids

PHOSPHODYESTERASE-4 INHIBITORS ANTI-

Roflimulast INFLAMMATORY
TREATMENT
OPTIONS
OTHER MEDICINES
Mucolytics

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Budesonide
Fluticasone

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CORTICOSTEROIDS ICSs are the MAIN TREATMENT of ASTMA!

• The effects of inhaled corticosteroids (ICS) in COPD are much less than in asthma.
Today, ICSs are used in patients with end-stage COPD (those with eosinophilia or those who cannot
be controlled with combined bronchodilator therapy) !!!

• Long-term treatment with an inhaler or oral corticosteroid alone is not

recommended.

• Oral corticosteroids are recommended for the treatment of only “COPD

exacerbation” at a dose of 40 mg / day for 5 days (more will not work! It increases
the risk of complications!).

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 Teaching
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 Corticosteroid Side Effects
Inhaled Steroids: Systemic Steroids :
• Myopathy
• Oral candidiasis • Obesity
• Hoarseness of voice • Hypertension
• Increased risk of pneumonia. • Psychiatric problems
• Decrease in bone densitometer. • Diabetes mellitus
• Osteoporosis
• Skin thinning and ecchymosis

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Pharmacological Treatment of Stable COPD

BRONCHODILATORS MAIN
TREATMENT
Anticholinergics (antimuscarinic), Beta 2 agonists, Methylxanthines OPTION

CORTICOSTEROIDS
Systemic corticosteroids, Inhaled corticosteroids

PHOSPHODYESTERASE-4 INHIBITORS ANTI-

Roflimulast INFLAMMATORY
TREATMENT
OPTIONS
OTHER MEDICINES
Mucolytics

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 Phosphodiesterase-4 Inhibitors
• The group of drugs with anti-inflammatory effects are
phosphodiesterase-4 inhibitors.

Roflumilast;
• Roflimulast is used in those with FEV1 below 50% and those with
Chronic bronchitis.
• In selected patients with chronic bronchitis symptoms and frequent
flare-ups it may reduce exacerbations

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 MUCOLYTICS

• Controversial use in COPD

• Generally, mucolytics are not recommended for use in stable
COPD treatment.
Side effects;
• Nausea
• Vomiting
• Fever
• Rhinorrhea
• Bronchoconstriction
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WHO: World health organization

CDC: Center of diseases control
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Comorbidities

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Comorbidities

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COPD EXACERBATIONS
Dr Ayse Baha
Near East University Faculty of Medicine
Phase 4 (2024-2025)
Definition of Exacerbation

• Exacerbation = Flare up= Attack

• It is an acute event
• Worsening of the patient's respiratory tract symptoms beyond the
daily observed normal change and leading to a change in medication.

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COPD exacerbation

• Episodes of increasing
respiratory symptoms
(ANTHONISEN CRITERIA)
• Dyspnea and/or
• Cough and/or
• Sputum production and/or
• Sputum purulence and/or
• Consequences!
Clinical Features
• Dyspnea: Progressive, persistent and worsen with exercise
• Chronic cough: may be in termitten and productive
• Sputum production (yellow, green, grey)
• Wheezing
• Chest tightness
Etiology of Exacerbations

• 80% tracheobronchial infections

bacterial agents 40-50%, viral agents 30-40%, atypical bacterial agents 5-10%
• 20% Noninfectious

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Non-infectious etiology
• Heart failure
• Pulmonary embolism
• Pneumothorax
• Smoking
• Treatment noncompliance (inhaler, oxygen, NIV)
• Cold weather
• Air pollution
• Allergens
Which patient has frequent exacerbations?

• Frequent exacerbation phenotype (≥2 exacerbations/year)

• Not avoiding risk factors
• Severe emphysema
• Chronic bronchitis phenotype
• Airway wall thickening (CT finding)
Factors that increase the risk of mortality
1. Advanced age
2. Low BMI (body mass index)
3. Comorbidities (cardiovascular diseases, DM, lung cancer, etc.)
4. Frequent hospitalization
5. LTOT (oxygen at home) use
6. Severe symptoms and poor quality of life
7. Significant loss of lung function
 DIAGNOSIS

COPD exacerbation is diagnosed

clinically.

There is no diagnostic test (there are

tests that help with differential
diagnosis)

If there is an increase in symptoms and

compatible physical examination
findings, we should consider a COPD
exacerbation.

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VAS (visual analog scale)

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Classification of
Severity of COPD
Exacerbations

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 We should decide where to perform the
treatment!

• Home? • Hospital?
• Ward
• Intensive Care

Assess exacerbation
• Is it life-threatening? (respiratory failure?)
• Is respiratory workload increased? (accessory muscles using?)
• Is gas exchange impaired? (arterial blood gas?)
 Respiratory Failure Description

no respiratory failure Non-life-threatening acute respiratory failure

1. RR 20-30/min 1. RR >30/min
2. Accessory respiratory muscles are not used 2. Accessory respiratory muscles are used
3. No change in mental status 3. No change in mental status
4. Hypoxemia improves with oxygen therapy 4. Hypoxemia improves with oxygen therapy
5. PaCO2 is normal 5. Hypercarbia (PaCO2 50-60 mmHg)

Life-threatening acute respiratory failure

1. RR >30/min
2. Accessory respiratory muscles are used
3. There is acute deterioration in mental status
4. Hypoxemia does not improve with oxygen therapy (FiO2 >40% with Venturi mask)
5. Hypercarbia and acidosis (PaCO2 >60 mmHg, pH ≤7.25)
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 Indicators for Home Treatment

• If there is a response to the initial treatment in the emergency room,

• If the mental status is normal,
• If there is no hypoxia,
• If there is no need for NIV or IMV,
• If the hemodynamics are stable (blood pressure, pulse),
• If there is social support at home,
• If there is no serious comorbidity, the patient can receive treatment at home.
Emergency treatment
for severe but non-life-threatening exacerbations
• Evaluate symptoms, ABG and chest X-ray
• Oxygen therapy if need
• Short-acting bronchodilator therapy (with nebulizer)
- Short-acting beta2-agonist
- Add short-acting anticholinergic to therapy if necessary (combined
therapy)
If the patient is comfortable, treatment
• Systemic corticosteroid (40 mg prednisolone IV) can be continued at home.
• NIMV (if need) If there is no response to initial
• Embolism prophylaxis treatment, treatment should be done in
hospital.
• Treatment of comorbid diseases
• (e.g. heart failure, arrhythmias, pulmonary embolism, infection, etc.)
• Theophylline iv (last option)
Home Treatment
• Antibiotic treatment (5-7 days)
• Macrolide
• Coamoxiclav
• Adjustment of bronchodilator treatment (SABA, SAMA)
• Inhaler or nebuliser
• SABA inhaler 4x2 pufs and/or SAMA inhaler 4x2 pufs
• SABA nebuliser 4x1 and/or SAMA nebuliser 4x1
• Oral corticosteroid (0.5 mg/kg methylprednisolone – 5 days)
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NIV: Positive Airway Pressure (PAP) Teaching
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Good luck…

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