Chronic Obstructive Pulmonary Disease (COPD) is a preventable lung disease characterized by airflow limitation caused by chronic inflammation. It includes chronic bronchitis and emphysema. Key risk factors include cigarette smoking and air pollution. Diagnosis involves assessing symptoms, lung function tests showing airflow limitation, and ruling out other conditions. Management focuses on smoking cessation, vaccinations, bronchodilators, corticosteroids, pulmonary rehabilitation, and oxygen therapy for severe disease.
3. COPD
• Also known as
COLD (Chronic Obstructive Lung Disease )
COAD (Chronic Obstructive Airway Disease)
Smoker’s lung
CAL (Chronic Airflow Limitation)
CORD (Chronic Obstructive Respiratory Disease)
4. Definition
Chronic obstructive pulmonary disease
(COPD) is a preventable and treatable disease
characterized by airflow limitation that is
progressive, not fully reversible and
associated with an abnormal inflammatory
response of the lungs.
5.
6. Chronic Bronchitis
• Chronic bronchitis is a
chronic inflammatory
condition in the lungs
• It causes a cough that
often brings up mucus, as
well as shortness of
breath,wheezing, and
chest tightness
7. Emphysema
• In emphysema, there is
over-inflation of the air
sacs (alveoli) in the
lungs, causing a
decrease in lung
function, and often,
breathlessness. It
involves destruction of
the lungs.
8. Epidemiology
• More common in older people, especially
those >65 years.
• Fifth leading cause of death and disability
worldwide.
• Death rates for males and females are roughly
equivalent.
• COPD mortality has also increased compared
with heart and cerebrovascular disease over
the same period.
10. Risk Factors
• Exposures:
– Cigarette smoking
(tobacco exposure)
accounts for 85% to
90% of cases of COPD.
– Air pollution and
occupational exposures
result in inflammation
and cell injury which
leads to COPD.
11. Host Factors
• Host factor refers to the traits of an individual
person that affect susceptibility to disease.
– AAT deficiency accounts for less than 1% of COPD
cases.
– Airway hyperresponsiveness due to various
inhaled particles may cause an accelerated decline
in lung function.
– Impaired lung growth due to low birth weight,
prematurity at birth, or childhood illnesses.
12. Pathophysiology of COPD
1. Airway inflammation
2. Structural changes
3. Mucociliary dysfunction
- Chronic inflammatory cascade for COPD
15. Clinical Presentation
Physical
History Examination
- Cyanosis of mucosal
- Symptoms: Cough, membranes
dyspnea, sputum, - Barrel chest
wheezing - Increased resting
- Smoking history, respiratory rate
environmental and - Shallow breathing
occupational risk - Pursed lips during
factors expiration
- Use of accessory
respiratory muscles
16. Diagnostic Testing
• Pulmonary function testing or
Spirometry
– Comprehensive assessment of lung
volumes and capacities
– Performed in all patients suspected
of COPD
– FEV1 defines the severity of
expiratory airflow obstruction and is
a predictor of mortality
• Bronchodilator reversibility:
– A large increase in post-
bronchodilator FEV1 supports the
diagnosis of asthma
17.
18. Diagnostic Testing
• Laboratories:
– ABG Monitoring:
• Done for patients with severe COPD, respiratory failure
or a severe exacerbation
– ATT levels (1.5 - 3.5 gram / liter):
• Measured in young patients who develop COPD and
have a strong family history.
• A serum value <15–20% of the normal limits is highly
suggestive of α1-antitrypsin deficiency.
19. Diagnostic Testing
• Imaging:
– Chest radiographs
• Not sensitive for the diagnosis of COPD
• Helpful in excluding other diseases (pneumonia, cancer,
congestive heart failure, pleural effusion &
pneumothorax)
– Chest CT
• For patients with severe COPD for lung volume
reduction surgery (LVRS) & lung transplantation.
20. COPD Management
• Goals of COPD Management:
– To relieve symptoms
– To improve quality of life
– To decrease the frequency & severity of acute
attacks
– To slow the progression of disease
– To prolong survival
24. Immunization
• Influenza vaccination
– Reduces the incidence of influenza-related acute
respiratory illness in COPD patients
– Patients with serious allergy to eggs should not be
given this vaccine.
– Brand available: Fluarix®
– An oral antiinfluenza agent (Oseltamivir) can be
given to such patients but its less effective and
causes more side effects.
– Available brand: Tamiflu®
25. Immunization
• Polyvalent pnuemococcal vaccine
– Recommended for all COPD patients
• 65 years and older
• Less than 65 years only if the FEV1 is less than 40%
predicted.
– Dosage: 0.5ml IM
– Available brand: Pneumovax® (0.5ml pre-filled
syringes)
26. Long-term Oxygen Therapy
• Should be started if
– Resting PaO2 is less than
55 mm Hg
– Evidence of right-sided
heart failure,
polycythemia, or impaired
neuropsychiatric function
with a PaO2 of less than
60 mm Hg
27. Pulmonary Rehabilitation
• Improves symptoms and
quality of life
• Reduces frequency of
exacerbations
• Components include:
– Exercise training
– Nutritional counselling
– Psychosocial support
29. Short-acting 2-agonists
• Stimulate adenyl cyclase to
increase the formation of cAMP
MOA which causes bronchodilation.
• Improve mucociliary clearance
Duration of action • 4 to 6 hours
Selective 2- • Albuterol (Ventolin®),
agonists levalbuterol, pirbuterol
Less selective 2- • Metaproterenol, isoetharine,
agonists isoproterenol, epinephrine
30. Short-acting Anticholinergics
• Competitively inhibit cholinergic
receptors in bronchial smooth
muscle, block Ach, with the net
MOA effect of reduction in cGMP, which
normally constrict bronchial smooth
muscle.
Duration of • 4 to 6 hours, slower onset of
action in comparison to -
action agonists
• Ipratropium (Atrovent®,
Examples Atem®)
• Atropine
31. Long-acting 2-agonists
• Same as that of short-acting
MOA 2-agonists
Duration • 12 hours
of action
• Salmeterol (Serevent®)
Examples • Formoterol
• Arformoterol
32. Long-acting Anticholinergics
• Same as that of short-acting
MOA anticholinergics
Duration • Cause bronchodilation within 30
minutes, which persists for 24 hours,
of action allowing once daily dosing
Example • Tiotropium
33. Combination Anticholinergics & 2-
agonists
• Combining bronchodilators
with different MOA allows
reduced doses to be
administored, reducing
side effects.
• Albuterol and Ipratropium
available as an MDI
Combivent®
34. Methylxanthines
• Produce bronchodilation by:
MOA • Inhibition of PDE, increasing cAMP levels
• Inhibition of calcium ion influx into
smooth muscle
• Prostaglandin antagonism
• Stimulation of endogenous
catecholamines
• Inhibition of release of mediators from
mast cells and leukocytes
Therapeutic • 8-12 mcg/ml
Serum Levels
35. Methylxanthines
• Minor side effects:
– dyspepsia, nausea, vomiting, diarrhea, headache,
dizziness, tachycardia
• Serious toxic effects:
– arrhythmias and seizures
• Considered in patients who donot respond
well to bronchodilators
36. Corticosteroids
• Mechanism of Action
– Reduction in capillary permeability to decrease mucus
– Inhibition of release of proteolytic enzymes from
leukocytes
– Inhibition of prostaglandins
• ICS: Beclomethasone (Bekson, Clenil-A, Clenil
Forte, Rinoclenil), flunisolide, budesonide,
fluticasone, mometasone
• Systemic CS: Prednisolone (Deltacortil),
Methylprednisolone, Prednisone
37. Corticosteroids
• Inhaled CS
– Considered for symptomatic stage III or IV disease
who experience repeated exacerbation despite
bronchodilator therapy
• Systemic CS
– Short term use for acute exacerbations
– Not used in chronic management because of high
risk of toxicity
38. Combination ICS & Bronchodilators
• Effective in reducing the rate of COPD
exacerbations
• Reduces the number of total inhalations
needed, more patient compliance
• Available combination:
– Beclomethasone with salbutamol (Clenil
Compositum®)
– Budesonide with formeterol
– Fluticasone with salmeterol
39. AAT Replacement Therapy
• Considered for patients with AAT deficiency
• Life time treatment
• Therapy consists of giving a concentrated form
of AAT, derived from human plasma.
• The recommended dosing regimen for
replacing AAT is 60 mg/kg administered IV
once a week.
40. Indacaterol
• Indacaterol is an ultra-long-acting beta-
adrenoceptor agonist
• Approved by FDA on July 1, 2011
• Requires once daily dosing, unlike other long-
acting
• In clinical trials, the most common adverse
events were runny nose, cough, sore throat,
headache, and nausea.
• Recommended dose is one capsule (75mcg) per
day.
Overview of Management
41. Devices used in COPD
• Inhalers
• Small, handheld devices that deliver a puff of
medicine into the airways.
• Metered-dose inhalers (MDIs)
• Dry powder inhalers (DPIs) or breath
activated inhalers
• Inhalers with spacer devices
42. Metered-dose Inhalers
• Contains a liquid
medication delivered as
an aerosol spray.
• Quick to use, small, and
convenient to carry.
• Needs good co-
ordination to press the
canister, and breathe in
fully at the same time
43. Breath-activated inhalers
or DPI
• It releases a puff of dry
powder instead of a
liquid mist
• Require less co-
ordination than the
standard MDI.
• Slightly bigger than the
standard MDI.
• Example: Rotahaler
44. Inhalers with spacer devices
• Spacer devices are
used with pressurised
MDIs
• The spacer between
the inhaler and the
mouth holds the drug
like a reservoir when
the inhaler is pressed.
45. Nebulizers
• Nebulisers are
machines that turn the
liquid medicines into a
fine mist, like an
aerosol.
• Useful in people who
are very breathless e.g.
In severe attack of
COPD
• They are not portable
46. References
• BMJ Best Practices
• American Thoracic Society COPD guidelines
• The Washington’s manual of medical
therapeutics
• Pharmacotherapy : A pathophysiologic
approach, Joseph T. DiPiro
• Respiratory care pharmacology, Rau, Joseph
Notes de l'éditeur
Asthma just might pave the way for the development of chronic obstructive pulmonary disease (COPD), a much more serious lung condition.As a matter of fact, people with asthma are 12.5 times more likely to develop COPD later in life
Currently, three medications have been approved for smoking cessation: nicotine, bupropion, and varenicline.Nicotine replacement medications include 2- and 4-mg nicotine polacrilex gum, transdermal nicotine patches, nicotine nasal spray, the nicotine inhaler, and nicotine lozenges. All seem to have comparable efficacy but, in a randomized study, compliance was greatest for the patch, lower for gum, and very low for the spray and the inhaler.[93] A smoker should be instructed to quit smoking entirely before beginning nicotine replacement therapies.Optimal use of nicotine gum includes instructions to chew slowly, to chew 8 to 10 pieces/day for 20 to 30 minutes each, and to continue long enough for the smoker to learn a lifestyle without cigarettes, usually 3 months or longer. Side effects of nicotine gum are primarily local and can include jaw fatigue, sore mouth and throat, upset stomach, and hiccups.Several different transdermal nicotine preparations are marketed—three deliver 21 or 22 mg over a 24-hour period, and one delivers 15 mg over a period of 16 hours. Most brands have lower-dose patches for tapering. Patches are applied in the morning and removed either the next morning or at bedtime, depending on the patch. Patches intended for 24-hour use can also be removed at bedtime if the patient is experiencing insomnia or disturbing dreams. Full-dose patches are recommended for most smokers for the first 1 to 3 months, followed by one to two tapering doses for 2 to 4 weeks each. Nicotine nasal spray, one spray into each nostril, delivers about 0.5 mg nicotine systemically and can be used every 30 to 60 minutes. Local irritation of the nose commonly produces burning, sneezing, and watery eyes during initial treatment, but tolerance develops to these effects in 1 to 2 days. The nicotine inhaler actually delivers nicotine to the throat and upper airway, from where it is absorbed similarly to nicotine from gum. It is marketed as a cigarette-like plastic device and can be used ad libitum.Most recently, nicotine lozenges have been marketed over the counter. The lozenges are available in 2- and 4-mg strengths and are to be placed in the buccal cavity where they are slowly absorbed over 30 minutes.[94] Smokers are instructed to choose their dose according to how long after awakening in the morning they smoked their first cigarette (a measure of the level of dependence). Those who smoke within 30 minutes are advised to use the 4-mg lozenge, whereas those who smoke their first cigarette at 30 or more minutes are advised to use the 2-mg lozenges. Use is recommended every 1 to 2 hours.Nicotine medications seem to be safe in patients with cardiovascular disease and should be offered to them.[95–98] Although smoking-cessation medications are recommended by the manufacturer for relatively short-term use (generally 3–6 mo), the use of these medications for 6 months or longer is safe and may be helpful in smokers who fear relapse without medications.
Bupropion sustained release, a dopamine-norepinephrine reuptake inhibitor that also has nicotinic cholinergic receptor antagonist activity, was originally marketed and is still widely used as an antidepressant. Bupropion was found to aid smoking cessation independent of whether a smoker was depressed or not.[99] Hurt and coworkers[99] demonstrated that with a 300-mg sustained-release dose, 44% of patients quit at 7 weeks versus 19% of controls. n additional randomized, placebo-controlled trial demonstrated that the combination of bupropion with a nicotine patch is safe, and that bupropion alone or in combination was as effective or more effective than the patch alone.Bupropion in excessive doses can cause seizures and should not be used in an individual with a history of seizures or with eating disorders (bulemia or anorexia).Varenicline, available by prescription only, is a nicotinic receptor partial agonist that selectively binds to α4β2 nicotinic cholinergic receptors in the brain.[102] This receptor mediates dopamine release and is thought to be the major receptor involved in nicotine addiction. A partial agonist means that the drug both activates the receptor and blocks the effects of other agonists on the receptor. Varenicline activates the α4β2 nicotinic cholinergic receptor with a maximal effect about 50% that of nicotine and, at the same time, blocks effects of nicotine from tobacco use on the receptor. As a consequence of the receptor stimulation, nicotine withdrawal symptoms are relieved, and as a consequence of receptor blockade, the rewarding effects of smoking are diminished. The latter effect reduces the desire to smoke and, in the case of a lapse, may prevent continued smoking.Varenicline's mechanism of action. (A) Nicotine from cigarettes stimulates the production of high levels of dopamine in terminal synapse in the nucleus accumbens. (B) No nicotine present, which induces a state of nicotine withdrawal. (C) Varenicline blocks the nicotine-receptor sites and partially agonizes the receptors, stimulating moderate levels of dopamine in the terminal synapse in the nucleus accumbens.
Doses & Administrations: AVIAN FLU & INFLUENZA:ADULT DOSE:MILD CASES : 75 mg bid x 5 daysSEVERE CASE: 150 mg bid x 7-10 daysPROPHYLAXIS: 75 mg QD x 7-10 days for avian flu and up to 6weeks for influenzaAdverse Effects: Nausea, vomiting, insomnia, bronchitis
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Has no direct effect on lung function or gas exchange. Optimizes other body systems so that the impact of poor lung function is minimized.
Replacement therapy consists of giving a concentrated form of AAT that is derived from human plasma. It raises the AAT level in the bloodstream. Once you start replacement therapy, however, you must undergo treatment for life. This is because if you stop, your lungs will return to their previous level of dysfunction and the neutrophil elastase will again start to destroy your lung tissue.
An episode of coughing soon after inhalation of the drug was observed in about a quarter of clinical trial participants during at least 20% of visits to study clinics. According to the labeling, the cough generally occurred within 15 seconds after inhaling 75 µg of indacaterol, lasted no more than 15 seconds, and was not associated with bronchospasm, COPD exacerbation or deterioriation, or reduced drug efficacy
