CHRONIC OBSTRUCTIVE PULMONARY DISEASE
MORPHOLOGY OF LUNGS
INTRODUCTION
• Chronic obstructive pulmonary disease is defined as a group of
diseases characterised by persistent slowing of airflow during
expiration.
• COPD is a syndrome of chronic Bronchitis and Emphysema.
• COPD is a disease state 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.
CHRONIC BRONCHITIS
It is defined as a clinical disorder charecterised by
excessive mucous secretions in the bronchial tree
manifested by chronic recurrent productive cough
for more than 3 months in a year for 2 consecutive
years.
EMPHYSEMA
It is defined as an anatomical alteration of the lung,
charecterised by abnormal enlargement of the
airspaces distal to the terminal, non-respiratory
bronchioles and accompanied by destructive changes
in the alveolar walls.
PATHOPHYSIOLOGY
• Mucous hypersecretion, ciliary dysfunction
and complications
• Airflow limitation and hyperinflation
• Gas exchange abnormalities
• Pulmonary hypertension
• Cor pulmonale
• Inflammation and skeletal muscle wasting
PATHOLOGICAL CHANGES
• Effect 4 different compartments of lungs:
• Central airways
• Peripheral airways
• Lung parenchyma ( Bronchioles, alveoli,
capillaries)
• Pulmonary vasculature
BRONCHIAL WALL
CHRONIC BRONCHITIS
Excess mucous secretions
Inflamated lung endothelium
Damaged cilia
Tissue destruction
Airway obstruction
Decreases gas exchange
Infections
Hypoxemia
Pulmonary hypertension
Polycythemia
EMPHYSEMA
Destructive enlargement of air sacs
Dilation and destruction
Impaired gas exchange
Breakdown of elastin
Loss of elasticity
Lack of alpha1 anti trypsin
2 types
CENTRILOBULAR:
Dilation & destruction of bornchioles,
alveolar ducts, alveoli. In COPD
PANACINAR:
Destruction of whole acinus ( airway
ending). In alpha1 antitrypsin
deficiency.
PINK PUFFERS BLUE BLOATERS
EMPHYSEMA CHRONIC BRONCHITIS
STRUCTURAL CHANGES IN ALVEOLI
AETIOLOGY
1. Smoking
Major cause of COPD and risk increases
2. Age
Increasing age results in ventilatory impairment
3. Gender
Women have greater airway reactivity and experience faster
declines in FEV1 and are at more risk than men.
4. Occupation
Coal and gold mining, cement & cotton industries, farming
and grain handling.
Aetiology …
5. Genetic factor
Deficiency of α1 antitrypsin ( strongest risk factor)
Genetic disorders involving tissue necrosis factor,
Epoxide hydrolase ( secondary risk factors)
6. Air pollution
Death rates are higher in urban areas than in rural areas
Indoor air pollution from burning fuel biomass ( In underdeveloped areas)
7. Socio-economic status
More common in individuals of low socio-economic status
8. Airway- hyper responsiveness &allergies
Smokers show high IgE & eosnophils & airway hyper responsiveness
SYMPTOMS
• Chronic cough ( after 20 or > cigarettes/day)
• Dyspnea (during physical activity and rest)
• Frequent respiratory infections
• Production of purulent sputum
• Bluish discoloration of lips and nail beds
• Morning headaches
• Wheezing
• Weight loss
• Pulmonary hypertension
• Peripheral oedema
• Hemoptysis
DIAGNOSIS
• Medical history
• Physical examination
• Chest X-ray
• Chest radiographs
• CT scan
• Pulmonary function tests
• Measurements of O2 & Co2 in blood
• Listening to faint and distant breath sounds with a
stethescope
• Spirometry
• Oximetry
SPIROMETER
Lung function tests
For the assessment of airflow limitation through spirometer is
the standard for diagnosis and monitoring of COPD.
Stage Clinical state Investigation
Mild cough, little breathlessness FEV1 >80%
Moderate cough, breathlessness on
exertion FEV1 30-80%
Severe cough, breathlessness on
exertion, cyanosis, oedema FEV1 <30%
TREATMENT
Non pharmacological treatment
1. Smoking cessation
2. Domiciliary oxygen therapy
3. Pulmonary rehabilitation
4. Nicotine replacement
5. Bupropion amfebutamone( licensed antidepressant drug )
6. Pneumococcal vaccination
7. Health education
Pharmacological treatment
I. Sympathomimetics
β2 selective sympathomimetics cause relaxation of
bronchial smooth muscles and bronchodilation by
stimulating enzyme Adenyl cyclase to increase the
formation of Cyclic adenosine monophosphate
Improve Mucociliary clearence.
Administered as MDI, DPI, Nebulizer
DRUGS: Albuterol, Bitolterol, Pirbuterol, Terbutaline
Formoterol, Salmeterol
Short acting agents
Rapid relief, less side effects, greater Beta 2 selectivity
Salbutamol 2-4mg oral
Inh. 100-200µg 3-4 times daily
Terbutaline 5mg oral
Long acting agents
When patient remain symptomatic and demonstrate frequent need of short
acting agents
Inh. Salmeterol 25µg bid
Inh. Formeterol 12-24µg bid
Adverse effects:
Headache
Tachycardia
Peripheral vasodilation
Nervousness
II. Anticholinergics
These agents produce bronchodilation by inhibiting cholinergic
receptors in Bronchial smooth muscle. This activity blocks ACH,
with a net effect being a reduction in Cyclic guanosine
monophosphate, which constricts bronchial smooth muscle.
Slow acting agents
Ipratropium bromide 20-40µg 3-4 times daily
Long acting agents
Tiotropium bromide ( 1 capsule once a day using
Handihaler inhalation device)
Adverse effects:
Dry mouth
Urinary retention
Blurred vision
Constipation
III. Methyl xanthines
Produce bronchodilation by inhibition of
phosphodiesterase ( there by increase in cAMP levels) and
inhibition of calcium ion influx into smooth muscles,
Prostaglandin and Adenosine receptor antagonism,
Stimulation of endogenous catecholamine's, Inhibition of
mediators release from Mast cells and Leucocytes.
• Theophylline ( Sustained released are preferred)
Initiated with200 mg twice a day & titrated to target
dose for every 3-5 days
• Aminophylline
FACTORS THAT DECREASE FACRORS THAT INCREASE
THOEPHYLLINE CLEARENCE THEOPHYLLINE CLEARENCE
• Advanced age • Tobacco
• Bacterial or Viral Pneumonia • Marijuana smoking
• Heart failure • Hyper thyroidism
• Liver dysfunction • Drugs: Phenytoin
• Hypoxemia Phenobarbital
• Drugs: Cimetidine Rifampin
Macrolides
Flouro quinolone AB
Adverse effects:
Irritation
Dyspepsia
Diarrhoea
Insomnia
Nausea
Vomiting
Head ache
Seizures
Palpitation
Tachycardia
Arrhythmias
IV. Corticosteroids
Used for moderate to severe COPD( FEV1 < 50%)
• Decrease mucous production
• Inhibition of release of proteolytic enzymes from
leukocytes
• Inhibition of prostaglandins
Prednisolone-40-60mg
Inh. Beclomethasone dipropionate 300-800µg in 2-4 div doses
Inh. Budesonide 200-800µg in 2 div doses
Inh. Fluticasone 200-500µg in 2 div doses
Adverse effects:
Inhaled corticosteroids
Hoarseness
Oral candidasis
Adrenal suppression
Oral corticosteroids
Cushing syndrome
Osteoporosis
Precipitation diabetes
Peptic ulceration
COMBINATION THERAPY
• Albuterol & Ipratropium( COMBIVENT)
MDI for chronic maintenance therapy
• Salmeterol & Fluticasone
• Formoterol& Budesonide
Will improve FEV1, excacerbation frequency
V) ANTIBIOTICS
If purulent sputum & acute infective exacerbations
are observed
PATHOGENS:
Streptococcus pneumonia
Staphylococcus aureas
Haemophilus influenzae
Moraxella catarrhalis
DRUGS
Co-Amoxiclav, Amoxicillin
Erythromycin, Doxycycline
Flucloxacillin
If the purulent sputum is still present after 1 week of treatment
sputum should be cultured for the identification of pathogen.
PROPHYLACTIC IMMUNIZATION
• Single dose of Pneumonococcal vaccine & annual
influenza vaccinations
• Prevalent strains of influenza change so the vaccine
composition is, correspondingly, altered annually
• Immunization has been shown to reduce
hospitalizations and risk of death in elderly with
chronic lung disease.
TREATMENT OF ACUTE EXACERBATIONS
• Domiciliary Oxygen therapy ( Cor pulmonale)
• Non invasive positive-pressure ventilation
• Bronchodilators (MDI or nebulisation)
• Theophylline ( if not responded to other
therapies)
• Corticosteroids (9 – 14 days, IV or oral)
• Antimicrobial therapy ( Initiate within 24 hrs
and continue for 7- 10 days)
PATIENT COUNSELLING
• Advice and support on stop smoking
• Nutritional assessment
• Aerobic exercise training
• Breathing training with closed lips to improve
ventilatory pattern and gas exchange.
• Relaxation techniques
• Education about medicines, nutrition, self-
management of disease and lifestyle issues
• Psychological support
Follow the 5A Strategy
• ASK (about tobacco use)
• ASSESS (the status and severity of use)
• ADVISE (to stop)
• ASSIST (in smoking cessation)
• ARRANGE (follow-up programme)
THANK YOU
