COPD is characterized by non-reversible airflow limitation caused by an abnormal inflammatory response to noxious particles or gases. The two most common conditions are chronic bronchitis and emphysema. Pharmacological treatments aim to relieve symptoms, prevent disease progression, and improve health outcomes. Therapies include bronchodilators, corticosteroids, vaccines, antibiotics, and supplemental oxygen. Managing exacerbations focuses on reversing acute symptoms and respiratory failure through bronchodilators, corticosteroids, and ventilation support.

1. COPD
Presented by : Anum Abdul Sattar
M.pharm(pharmacy practice)
Ist semester

2. DEFINITION:
(COPD) :-
 characterized by non reversible
airflow limitation .
 The airflow limitation is usually
progressive and associated with an
abnormal inflammatory response of
the lungs to noxious particles or
gases.
 common conditions in COPD :chronic
bronchitis and emphysema.

3. CHRONIC BRONCHITIS:-
 chronic / recurrent excess mucus secretion
in bronchial tree with cough occurring mostly
for at least 3 months of the year and at least
2 consecutive years when other causes of
cough have been excluded.
EMPHYSEMA: -
 abnormal, permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls, but
without obvious fibrosis.(formation of excess
fibrous connective tissue in organ/tissue as a
reparative process)

4. SYMPTOMS

6. CAUSES

7. PATHOPHYSIOLOGY

8.  noxious particles and gases stimulates the activation of
neutrophils,macrophages, and CD8+ lymphocytes,
which release a variety of chemical mediators, including
tumor necrosis factor-α, interleukin-8,and leukotriene
B4. These inflammatory cells and mediators lead to
widespread destructive changes in the airways,
pulmonary vasculature,and lung parenchyma.
 oxidative stress ,imbalance between aggressive and
protective defense systems in the lungs (proteases and
antiproteases). Increased oxidants generated by
cigarette smoke react with and damage various proteins
and lipids, leading to cell and tissue damage. Oxidants
also promote inflammation directly and exacerbate the
protease-antiprotease imbalance by inhibiting
antiprotease activity.

9.  The protective antiproteaseα1-antitrypsin
(AAT) inhibits several protease enzymes,
including neutrophil elastase. In the presence
of unopposed AAT activity, elastase attacks
elastin, which is a major component of
alveolar walls. A hereditary deficiency of AAT
results in an increased risk for premature
development of emphysema. Activated
inflammatory cells release several other
proteases, including cathepsins and
metalloproteinases. In addition, oxidative
stress reduces antiprotease (or protective)
activity.

10. CLINICAL PRESENTATION

11. DIAGNOSIS

12. .

13. PULMONARY FUNCTION TEST
 Spirometry standard for diagnosing and
monitoring COPD
 Establishing of COPD diagnosis: FEV1 (The
forced expiratory volume after 1 second) /
forced vital capacity (FVC) ratio ≤0.7,
demonstrating airflow limitation that is not fully
reversible.
 based on SPIROMETRY, severity measured,
assessed
 Patients classified by severity of airflow
obstruction (Grades 1–4) then into Group (A,
B, C, or D) based on the impact of symptoms
and risk for future exacerbations.

14. ARTERIAL BLOOD GASES
 Patients with severe COPD can have a low arterial
oxygen tension (PaO2 45 to 60 mm Hg) and an
elevated arterial carbon dioxide tension (PaCO2 50 to
60 mm Hg).
 The diagnosis of acute respiratory failure in COPD is
made on the basis of an acute drop in PaO2 of 10 to 15
mm Hg / acute increase in PaCO2 that decreases
serum pH 7.3 /less.
 If acute respiratory distress develops (e.g.pneumonia
/COPD exacerbation) the PaCO2 may rise sharply
resulting in an uncompensated respiratory acidosis
 Respiratory acidosis is a condition that occurs when the
lungs can't remove enough of the carbon dioxide (CO2)
produced by the body. Excess CO2 causes the pH of blood
and other bodily fluids to decrease, making them too acidic.

15. TREATMENT
 Prevent disease progression
 Relieve symptoms
 Improve exercise tolerance
 Improve health status
 Prevent and treat exacerbations
 Reduce mortality

16. THERAPEUTIC PLAN
 Approaches to treatment:
1. Pharmacotherapy
2. Non pharmacological therapy
3. Surgical management
4. Managing exacerbations
 Improving outcomes

17. NON PHARMACOLOGICAL
THERAPY

18. PHARMACOTHERAPY
 The current pharmacological treatment of COPD
is symptomatic
1. it is mainly based on:
I. bronchodilators : selective β2-adrenergic agonists
(short- and long-acting)
II. Anticholinergics
III. Methyl xanthines
IV. combination of these drugs.
V. Corticosteroids
2. other types of medication (vaccines,
antibiotics,α1- anti trypsin augmentation
therapy, mucolytic agents, antioxidants,
immunoregulators, antitussives and
vasodilators).

19.  Treat symptoms of low risk for exacerbations(Group A) :
short-acting inhaled bronchodilators .
 more persistent symptoms(Group B):long-acting inhaled
bronchodilators .
 For high risk for exacerbations (Groups C and D):
inhaled corticosteroids.
 Short-acting inhaled bronchodilators (β2-agonists or
anticholinergics) :initial therapy for patients with
intermittent symptoms;
 relieve symptoms and increase exercise tolerance.
 Long-acting inhaled bronchodilators (β2-agonists
[LABA] or anticholinergics) : moderate to severe COPD
when symptoms occur on a regular basis or when
short-acting agents provide inadequate relief.
 They relieve symptoms , reduce exacerbation frequency, and
improve quality of life and health status.

22. 1. BRONCHODILATORS

23. ii.ANTICHOLINERGICS
.

24. iii.METHYLXANTHINES

25. iv.CORTICOSTEROIDS

26. 2.OTHER THERAPIES
 vaccines
 antibiotics
 α1- anti trypsin augmentation therapy:
◦ Not recommended for patients with COPD
that is unrelated to genetic deficiency.
 mucolytic agents:
◦ Patients with viscous sputum may benefit
from mucolytics , overall benefits are small
 Immuno regulators
 Vasodilators:
◦ Nitric oxide is contraindicated in stable
COPD. The use of endothelium modulated
agents for treatment of pulmonary
hypertension associated with COPD is not
recommended

27.  Expectorants and mucolytics
◦ use of saturated solutions of potassium iodide, ammonium
chloride, acetylcysteine, and guaifenesin.
 Respiratory stimulants
◦ no role in long-term management
◦ some utility in the acute setting include almitrine and
doxapram.
 Narcotics
◦ Systemic (oral/parenteral)opioids(morphine), can relieve
dyspnoea for patients with end-stage COPD.
 Dietary supplements
◦ antioxidants (vit E ,C , β-carotene),reduce frequency of
exacerbations .may be beneficial in COPD as a result of an
imbalance between oxidants and antioxidants
 Surgical interventions
◦ bullectomy,
◦ lung volume reduction surgery
◦ (LVRS), and lung transplantation.
 Suppressive Anti microbial agents (to treat colonized

29. α1- ANTI TRYPSIN
AUGMENTATION THERAPY
 Used as an augmentation therapy in
patient with inherited AAT deficiency.
 To maintain the serum concentrations
above the protective threshold.
 Consists of weekly infusion of pooled
human AAT plasma level.

34. COPD EXACERBATION
 An exacerbation of COPD is defined as “an event
in the natural course of the disease characterized
by a change in the patient's baseline dyspnoea,
cough, and/or sputum and beyond normal day-to-
day variations, that is acute in onset and may
warrant a change in regular medication in a patient
with underlying COPD
 TREATMENT:
 The goals are to
◦ 1) prevent hospitalization or reduce length of
◦ hospital stay
◦ 2) prevent acute respiratory failure and death
◦ 3) resolve symptoms
◦ 4) return to baseline clinical status and quality of life.

36. MANAGING EXACERBATION:
 NON PHARMACOLOGICAL
THERAPY:
 oxygen therapy( for patients
with hypoxemia.)
 Non invasive positive
pressure ventilation:
◦ ventilatory support with
oxygen and pressurized
airflow using a face or
nasal mask without
endotracheal intubation.
 PHARMACOLOGICAL
THERAPY:
i)Bronchodilators ii)
corticosteroids iii) anti
microbial therapy

37. COMPLICATIONS
 Cor Pulmonale
◦ condition that causes the right side of the heart to fail.
◦ Long-term high blood pressure in the arteries of the lung
and right ventricle of the heart lead to cor pulmonale.
◦ High blood pressure in the arteries of the lungs is
called pulmonary hypertension.
 Treatment:
◦ Long-term oxygen therapy and diuretics
◦ Other pharmacologic agents:
 hydralazine,
 calcium channel blockers,
 angiotensin-converting enzyme inhibitors,
 angiotensin II antagonists.

38. POLYCYTHEMIA
 Condition
where hematocrit (the
volume
percentage of red
blood cells in
the blood) is
>55% due to an
increase in the RBC
number/decrease in
the volume of plasma
 treatment:
◦ phlebotomy (removal of
blood from the
circulation).
◦ oxygen therapy

39. INVESTIGATIONAL
THERAPY PDE4 INHIBITORS:
◦ block the degradative action
of PDE4 on CAMP by
hydrolyzing CAMP . Reduce
airway inflammation.

40. CONTROVERSY