COPD Flashcards
ACUTE BRONCHITIS
• Often Viral in previously healthy subjects; Bacterial Secondary infections (HiB, S. pneum)
more likely in smokers or COPD patients
• Irritating, non-productive cough with chest discomfort and tightness, wheezing, SOB
• Cough becomes productive with yellow/green sputum, Mild fever and Neutrophilia
• Disease improves spontaneously in otherwise healthy adults after 4-8 days
• Antibiotics (e.g. Amoxicillin) – Unknown if would improve recovery time in otherwise healthy
ACUTE BRONCHITIS Causative Organisms
• IE COPD – Haemophilus influenzae (11%), Streptococcus pneumoniae (10%), Moraxella
catarrhalis (10%), Haemophilus parainfluenzae (10%) and Pseudomonas (4%)
• Atypical Pneumonia – Mycoplasma, Chlamydia spp, Legionella, Coxiella, Bordetella, S aureus,
Enterococci spp, Pseudomonas, Klebsiella, HiB, E coli, Moraxella
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
• Third most common cause of death, fifth most common cause of disability
• Variety of clinical syndromes associated with Airflow Obstruction and Lung Parenchyma
disease; Co-existence of Chronic Bronchitis, Chronic Asthma, Emphysema
o Chronic Bronchitis – Cough/Sputum production most days 3/12 of 2 successive years
• Physiological correlations – Pink Puffers, Blue Bloaters
“Pink Puffers”
↑VA (Alveolar Ventilation)
Near normal PaO2 with normal/low PaCO2
Breathless but not cyanosed
“Blue Bloaters”
↓VA and PaO2 with ↑PaCO2
Cyanosed but not breathless; loss of
Hypercapnic drive, reliant on Hypoxic drive
NB: O2 therapy under caution
COPD Prognosis and Risk Factors
• Associated with other comorbidities (IHD, HTN, DM, HF, Cancer) and may be part of systemic
inflammatory processes
• Defined as disease state characterised by Airflow Limitation that is not fully reversible (C/f
Asthma); Limitation is progressive and associated with abnormal inflammatory response
• 90% of COPD due to smoking but only 10-20% of heavy smokers get COPD – Indicates
individual susceptibility; Disease development is proportional to number of cigarettes/day
• COPD mortality increases during periods of heavy air pollution
• Poorer prognosis with Age and ↓FEV1; BODE (BMI,
Obstruction, Dyspnoea, ET) for mortality
Pathophysiology of COPD
• Increased numbers of Mucus Secreting Goblet cells in
Bronchial mucosa especially in larger bronchi; Overt
inflammation and pus in advanced disease
• Infiltration with Acute (e.g. Neutrophils) and Chronic (e.g.
Lymphocytes) Immune cells; Lymphoid follicles might develop in advanced disease
• Ulceration of Epithelial lining; Metaplasia of Squamous Respiratory Epithelium with Columnar
• Scarring and thickening of smaller airways; particularly affected in early disease although does
not cause SOB; reversible only in early smoking cessation
Emphysema
• Emphysema – Abnormal, permanent enlargement of air spaces distal to Terminal Bronchiole,
accompanied by destruction of Alveolar walls without obvious fibrosis
o Secondary to Small Airway Inflammation and Destruction
o Centri-acinar – Concentrated around Respiratory Bronchioles, Distal components well
preserved; Extremely common and not always leads to disability
o Pan-acinar – Whole Acinus; Severe Airflow Limitation and V/Q mismatch; Associated
with α1-Antitrypsin Deficiency, less common
o Irregular – Lung parenchyma independent of Acinar structure
• Emphysema leads to loss of Elastic Recoil = Increased Total Lung Capacity and Residual
Volume; Premature closure of airways limit expiratory flow; Loss of Alveoli leads to decreases
gas transfer; V/Q Mismatch due to damage and mucus plugging of smaller airways due to lack
of elastic support; Fall in PaO2 and Increased work of respiration
• Emphysema, Inflammation and Scarring of Small Airways and Mucus secretion all contribute
to hyperinflation of the lungs, V/Q mismatch, Increased work of breathing and SOB
Hypercapnic and Hypoxic Drive
• CO2 excretion less affected by V/Q mismatch initially, however with advanced disease CO2
retention can occur as part of Type 2 Respiratory Failure
• Short term – Patients might increase rate of respiration to combat rise in CO2
• Long term – Patients might become insensitive to CO2 (Main driver of respiration in healthy
people); Such patients might appear less breathless
o Renal Hypoxia – Fluid retention; Increased Erythropoietin = Polycythaemia
o Leads to Bloating, Plethora, Cyanosis = Blue Bloaters
• Administration of oxygen dangerous – Loss of
Hypoxic drive can lead to hypoventilation
Pathogenesis of COPD
• Cigarette Smoking – Causes immune response
which includes secretion of Elastases which lead to
Emphysema; Cigarette smoke also inhibits α1-
Antitrypsin; Mucus Gland Hypertrophy in the
Larger Airways as a response to smoke
• α1-Antitrypsin Deficiency – α1-Antitrypsin normally inhibits Proteolytic enzymes e.g.
Neutrophil Elastase, which breaks down Alveolar Wall Connective Tissue
o Can either be Homozygous or Heterozygous disease; 2% of Cases
o Suffers can also develop Liver Disease
Presentation of COPD
• Productive Cough with white/clear/grey Sputum, Wheeze and Breathlessness
• Frequent Exacerbations with Purulent Sputum
• Symptoms worsened with cold weather and pollution; In advanced disease ↓↓ETT
• Systemic effects – HTN, Osteoporosis, Depression, Weight Loss (Cachexia) and ↓Muscle mass
• Mild COPD might be asymptomatic; Hyperinflated lungs with poor Chest Expansion
• Hypercapnia – Peripheral Vasodilatation, Bounding Pulse, Flapping tremor (PaCO2>10kPa)
• Cor Pulmonale – Fluid overload secondary to Lung Disease
o In COPD, Peripheral Oedema and Fluid Retention due to Renal Hypoxia
o Cor Pulmonale is identified by Pulmonary Hypertension and RVH; Central Cyanosis,
SOB, Ankle Oedema; Parasternal Heave and P2 due to RVH
• Barrel-Chestedness – Might also be attributed to Osteoporosis of the Spine
Investigations for COPD
• Lung Function Tests – Airflow Limitation (FEV1:FVC
reduced, PEFR low); GOLD staging of COPD
• Carbon Monoxide Transfer Factor is low when
significant Emphysema is present
• CXR – Overinflation, Flattened Diaphragm; Presence
of Bullae, Large proximal vessels
• ↑Hb and PCV; Advanced disease may have T2RF at
rest on ABG
• Sputum – Commonly only S pneumo/HiB cause IECOPD; Moraxella occasionally; Chronic
colonisation makes culture not as useful
• ECG – Advanced disease (P Pulmonale in PHTN, RBBB and other evidence of RVH)
• α1-Antitrypsin levels and Genotyping for Premature disease, or lifelong Non-smokers
Smoking Cessation
• Smoking Cessation – Single most useful measure to slow down or prevent deterioration and
delay morbidity and mortality
• Nicotine gum and Transdermal Nicotine
• Varenicline – Selective Nicotinic Receptor Partial Agonist; Reduces cravings and decreases
pleasurable effects of tobacco products; 23% cessation after 1yr
• Bupropion (Amfebutamone) – Antidepressant, Mechanism not completely known;
modulation of Noradrenaline, Dopamine as well as Nicotinic Receptor Antagonist
Drug Therapy in COPD
• β2 Adrenergic Agonists – SABA for mild COPD;
LABA for more severe airflow limitation; either
as inhaler or inhaled powder
o Compound Bronchodilators e.g.
Combivent – Ipratropium and
Salbutamol
• Muscarinic Antagonists – More prolonged and
greater Bronchodilatation; Tiotropium (LAMA),
Ipratropium (SAMA); Increases function and
quality of life but does not affect decline;
Improvement might be small and can guide
whether or not to continue treatment
• Theophylline (PDE III Inhibitor) – Of little
benefit in COPD
• Phosphodiesterase IV inhibitors – E.g. Roflumilast as an adjunct to Bronchodilator therapy
• Corticosteroids – Steroid trial for patients with Moderate/Severe COPD; Proportion of
patients have a large reversible element to COPD and Airway Function might improve
o Prednisolone 30mg for 2 weeks with Lung Function Testing before and after
o If FEV1>+15%, Start on Inhaled Corticosteroids (e.g. Beclometasone); High Dose
Inhaled Steroids not advised as it increases risk of infection
• Antibiotics – Shortens episodes of IECOPD; Prevent Hospital admission and further damage
o Antibiotics kept at home and used as soon as Sputum turns Green/Yellow;
Amoxicillin± Clavulanic acid or Cephalosporins
• Antimucolytics – Reduce Sputum Viscosity, reduce AECOPD; 4-
week Trial of Carbocysteine
• Diuretic Therapy – Requires for all oedematous patients
• Oxygen Therapy – Continuous administration of O2 2L/min via
Nasal Prongs; Especially for patients with severe Hypoxaemia
(<7.3kPa), Polycythaemia, Cor Pulmonale etc
Nocturnal Hypoxia
• COPD with Severe Hypoxaemia may experience Profound Nocturnal Hypoxaemia particularly
during REM sleep; Desaturation to up 50% occurs; Secondary Polycythaemia exacerbated
• Alveolar Hypoventilation due to inhibition of intercostal/accessory muscles and shallow
breathing during REM sleep, Increased Upper Airway resistance due to reduce muscle tone
• Rise in Pulmonary Arterial Pressure due to Vasoconstriction; Most deaths at night possibly
due to Cardiac Arrhythmias due to Hypoxaemia
• Desaturation terminated by arousal from sleep causing poor quality of sleep
o Patients should not be given sleeping tablets as this worsens ↓Respiratory drive
o Treat with nocturnal O2 administration and Ventilatory support
• BiPAP (Inspiratory pressure for assistance, expiratory pressure to prevent closure) – Improves
ventilation during sleep, allows respiratory muscles to rest at night
