A brief presentation on chronic obstructive pulmonary disease Talking about epidemiology, pathophysiology, symptoms and the Gold standard treatment.

1. Chronic obstructive
pulmonary disease
Family medicine,
Madziga Adama.

2. DEFINITION
Chronic obstructive pulmonary disease (COPD) is the name for a collection of
lung diseases including chronic bronchitis, emphysema and chronic obstructive
airways disease. People with COPD have difficulties breathing, primarily due to the
narrowing of their airways, this is called airflow obstruction. COPD manifests via
chronic inflammatory response to irritants, frequently to tobacco smoke. The
progression of COPD from early onset to advanced disease leads to the loss of the
alveolar wall, pulmonary hypertension, and fibrosis of the respiratory epithelium.
Overall, the frequency of COPD ranges from 40–70% among lung
cancer patients, while smoking was found in 80–90% of lung cancer cases. Although
80–90% of COPD or lung cancer patients are smokers, only approximately 10% of
smokers develop lung cancer and approximately 20% develop COPD.
The good news is that COPD can often be prevented, mainly by not
smoking. Cigarette smoking is the leading cause of COPD. Most people who have
COPD smoke or used to smoke. However, up to 30% of people with COPD never
smoked. A rare genetic condition called alpha-1 antitrypsin (AAT) deficiency can also
cause the disease.

3. Chronic Bronchitis
Chronic bronchitis is a type of chronic obstructive pulmonary disease
(COPD) that is defined as a productive cough of more than 3 months occurring within a
span of 2 years. Patients typically present with chronic productive cough, malaise, and
symptoms of excessive coughing such as chest or abdominal pain. Chronic bronchitis is
thought to be caused by overproduction and hypersecretion of mucus by goblet cells.
Epithelial cells lining the airway response to toxic, infectious stimuli by
releasing inflammatory mediators such as interleukin 8 and other cytokines, which
results in air trapping, Hypoxemia and hypercapnia
During an acute exacerbation of chronic bronchitis, the bronchial
mucous membrane becomes hyperemic and edematous with diminished bronchial
muco-ciliary function. This, in turn, leads to airflow impediment because of luminal
obstruction to small airways. The airways become clogged by debris and this further
increases the irritation. The characteristic cough of bronchitis is caused by the copious
secretion of mucus in chronic bronchitis

4. Chronic
Bronchitis
increases the
chance of
Pneumonia
due to
infection
by H.fluenzae
and
M.cattarhalis.

5. Chronic Emphysema
• Pulmonary emphysema is a form of chronic obstructive pulmonary disease
that is defined as a pathological, permanent dilatation of distal airways
(respiratory bronchioles, alveolar ducts, and alveolar sacs) due to the
destruction of airway walls without fibrotic change. Emphysema interrupts
gas exchange, causing an obstructive ventilation defect.
Advanced emphysema is a common and serious cause of chronic
respiratory failure and acute decompensation that could be life-threatening.
Due to its high morbidity and mortality, recognizing and treating this
condition in its early stages is vital. Emphysema is differentiated from
interstitial pneumonia by the absence of fibrosis of the pulmonary
interstitium

6. •Emphysema is divided into the following subtypes
A] centrilobular emphysema; most common type of emphysema, classically seen in smokers and is
characterised by the destruction of the respiratory bronchiole (central portion of the acinus) but it
spares distal alveoli and usually affects the upper lobe
B] panlobular emphysema; this is a rare type of emphysema associated with α1-antitrypsin deficiency.
It is characterised by the destruction of the entire acinus (respiratory bronchioles and alveoli) and
usually affects the lower lobe.
Other subtypes include; cicatricial emphysema which is mainly caused by exposure to quartz dust
and results in chronic inflammation and nodular scar formation.
Giant bullous emphysema is characterised by large bullae (congenital or acquired) that extrude into
the surrounding tissue, the bullae may rupture leading to a pneumothorax and depending on the shape
of the bullae resection should be considered.
Senile emphysema is loss of pulmonary elasticity with age and may lead to emphysematous lung but
is not considered pathological but a normal consequence of ageing

9. Symptoms Of COPD
• Chronic cough
• Increasing breathlessness – this may only happen when exercising at
first, and you may sometimes wake up at night feeling breathless
• a persistent chesty cough with phlegm that does not go away
• frequent chest infections
• persistent wheezing.
RISK FACTORS OF COPD
• Smoking
• Age
• Environmental factors(pollutants, dust, silica)
• A1 antitrypsin genetic(autosomal dominant)

11. Classification
• GLOBAL INITIATIVE FOR CHRONIC OBSTRUCTIVE LUNG DISEASE
(GOLD) CLASSIFICATION
• GOLD classifies COPD according to the severity of airflow limitations
(GOLD 1-4) and the ABCD assessment tool, which takes into account
the modified British Medical Research Council (mMRC) dyspnea scale,
COPD assessment test (CAT), and the risk of exacerbation
• Classification based on airflow limitation in patients with FEV1/FVC <
70%. GOLD uses FEV1/FVC to classify COPD

14. TREATMENT
General treatment include;
A] Cessation of tobacco use
B] Pneumococcal vaccines and influenza vaccination; once before 65years of
age and once after
C] Pulmonary rehabilitation; indicated in patients with GOLD B,C and D and
include physiotherapy with breathing exercise
MEDICAL TREATMENT ACCORDING TO GOLD; medical treatment I COPD
reduces the severity of symptoms, improves overall health status and
lowers the frequency and severity of exacerbation. The first line of
treatment of COPD consists of bronchodilators, inhaled corticosteroids and
phosphodiesterase type 4 inhibitors
•Bronchodilators include; short acting beta agonist, long acting beta agonist,
short acting muscarinic antagonist and long acting muscarinic antagonist

15. Acute Exacerbation Management
To determine how bad a COPD exacerbation is, you look at response to therapy
•Give them O2 to get their SPO2 between 88-92%
•Give duo-nebulisers (both albuterol and ipratropium) every 30 minutes
•Steroids
After this there are 3 possible outcomes to determine the exacerbations; the patient gets
better, the patient gets worse or the patient needs more time for the therapy to improve
A] if patient gets better we give PO steroids and metered-dose inhalers of albuterol and
ipratropium
B] if patient gets worst meaning there is increased CO2, confusion, absence of wheezing or lung
sounds; they are given IV steroids (methylprednisolone) and nebuliser albuterol and ipratropium
moved to the ICU and are either put on BIPAP or an ET tube
C] if the patient needs more time, meaning no improves neither are they getting worst we can give
them either PO or IV steroids and nebulised albuterol and ipratropium
Most patients with COPD exacerbations need antibiotics such as azithromycin and doxycycline.
Azithromycin causes prolonged QT intervals so it is advised to get an ECG if time permits.