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COPD
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
BY
K.GOWRI PRIYA
19AB1T0011
PHARMD II
Introduction:
DEFINITION:
COPD is defined as a disease state characterised by the presence of airflow obstruction
due to chronic bronchitis or emphysema.The airflow obstruction is generally Progressively , may
be accompanied by airway hyper reactivity & may be partially reversible.
COPD is also known as chronic Obstructive lung disease (COLD), Chronic obstructive airway
disease (COAD), Chronic airflow limitation(CAL), Chronic Obstructive Respiratory Disease (CORD).
COPD refers to chronic bronchitis & Emphysema,a pair of 2 commonly co-existing diseases
of the lungs in which the airways become narrowed.This leads to limitation of the airflow.
AETIOLOGY:
◦ Cigarette Smoke.
◦ Genetics – Alpha 1 antitrypsin deficiency.
◦ Occupational exposure to chemicals.
◦ Ambient Air pollution.
◦ Sudden airway constriction in response to inhaled irritants.
◦ Bronchial hyper responsiveness.
TYPES OF COPD:
There are 2 types of COPD. They are:
1) Chronic bronchitis
2) Emphysema
(1). CHRONIC BRONCHITIS: It is a chronic inflammation of the lower respiratory tract
characterised by excessive mucous secretion , cough& dyspnea associated with recurrent
infections of the lower respiratory tract.
(Or)
Chronic bronchitis is inflammation (swelling) and irritation of the bronchial tubes. These tubes are
the airways that carry air to and from the air sacs in your lungs. The irritation of the tubes causes
mucus to build up.
TYPES OF COPD
(2) EMPHYSEMA :
It is a complex lung disease characterized by damage to the gas exchanging
surfaces of the lungs (alveoli).
(Or)
A disorder affecting the alveoli (tiny air sacs) of the lungs. The transfer of oxygen and carbon
dioxide in the lungs takes place in the walls of the alveoli. In emphysema, the alveoli become
abnormally inflated, damaging their walls and making it harder to breathe.
RISK FACTORS:
Risk factors for COPD include:
• Exposure to tobacco smoke. The most significant risk factor for COPD is long-term cigarette smoking. The more
years you smoke and the more packs you smoke, the greater your risk. Pipe smokers, cigar smokers and marijuana
smokers also may be at risk, as well as people exposed to large amounts of secondhand smoke.
• People with asthma. Asthma, a chronic inflammatory airway disease, may be a risk factor for developing COPD. The
combination of asthma and smoking increases the risk of COPD even more.
• Occupational exposure to dusts and chemicals. Long-term exposure to
chemical fumes, vapors and dusts in the workplace can irritate and inflame your lungs.
• Exposure to fumes from burning fuel. In the developing world, people
exposed to fumes from burning fuel for cooking and heating in poorly ventilated homes are at higher risk of
developing COPD.
• Genetics. The uncommon genetic disorder alpha-1-antitrypsin deficiency is the cause of some cases of COPD. Other
genetic factors likely make certain smokers more susceptible to the disease
CAUSES OF AIRWAY OBSERVATION:
Causes of airway obstruction include:
• Emphysema: This lung disease causes destruction of the fragile walls and elastic fibers of the
alveoli. Small airways collapse when you exhale, impairing airflow out of your lungs.
TYPES OF EMPHYSEMA:
In emphysema, the inner walls of the lungs’ air sacs (alveoli) are damaged, causing them to
eventually rupture. This creates one larger air space instead of many small ones and reduces the
surface area available for gas exchange.
1). Centrilobular emphysema : it is caused due to abnormal dilation or destruction of all
respiratory bronchioles the central position of the acinus.It is commonly associated with cigarette
smoking.
TYPES OF EMPHYSEMA:
2). Panacinar Emphysema : It refers to enlargement or destruction of all parts of the acinar it is
seen in alpha 1antitrpsin deficiency and in s.Panacinar emphysema : It refers to enlargement or
destruction of all parts of the acinar it is seen in alpha 1antitrpsin deficiency and in smokers.
TYPES OF EMPHYSEMA:
3). Paraseptal Emphysema:It usually involves the distal part of the secondary lobule the alveolar
ducts are predominantly affected.
PATHOPHYSIOLOGY:
Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible
airflow obstruction and an abnormal inflammatory response in the lungs. The latter represents the
innate and adaptive immune responses to long term exposure to noxious particles and gases,
particularly cigarette smoke.All cigarette smokers have some inflammation in their lungs, but
those who develop COPD have an enhanced or abnormal response to inhaling toxic agents. This
amplified response may result in mucous hypersecretion (chronic bronchitis), tissue destruction
(emphysema), and disruption of normal repair and defence mechanisms causing small airway
inflammation and fibrosis (bronchiolitis).
Molecular mechanisms of COPD Pathogenesis. Chronic exposure to noxious stimuli like
cigarette smoke produces differential effects on multiple lung cell types. The complexity of this
interaction produces lung remodeling that is both pro-fibrotic in airways and matrix-degrading in
the alveolar space.
PATHOPHYSIOLOGY:
PATHOPHYSIOLOGY:
◦ These pathological changes result in increased resistance to airflow in the small conducting
airways, increased compliance of the lungs, air trapping, and progressive airflow obstruction—
all characteristic features of COPD. We have good understanding of the cellular and molecular
mechanisms underlying the pathological changes found in COPD.
SYMPTOMS:
◦ COPD symptoms often don't appear until significant lung damage has occurred, and they
usually worsen over time, particularly if smoking exposure continues.
◦ Signs and symptoms of COPD may include:
◦ • Shortness of breath, especially during physical activities
◦ • Wheezing
◦ • Chest tightness
◦ • A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or
greenish
◦ • Frequent respiratory infections
◦ • Lack of energy
◦ • Unintended weight loss (in later stages)
◦ • Swelling in ankles, feet or legs.
Clinical manifestations of chronic bronchitis :
• Hypoxemia
• Hypercapnia
• Polycythemia
• Cyanosis
• Cor pulmonale
Clinical manifestations of Emphysema:
1).Early stages
1. Dyspnea
2. Non productive cough
3. Diaphragm flattens
4. Barrel chest
5. Respiratory alkalosis
2). Later stages
1. Hypercapnea
2. Purse lip breathing
3. Underweight
4. Lung sounds diminished
Your doctor will ask about your smoking history and listen to your lungs with a stethoscope.
You may take tests, including:
1. Pulmonary function tests: This is a series of measurements of how much air your lungs can hold
while breathing in and out.
2. Spirometry : The test measures two things :
•The most air you can breathe out after inhaling deeply.
The results will let you knowif you’re less able to breathe
normally.
•Exploratory ratio =FEV1/FVC.
How much air you can exhale in 1 second.
The score tells your doctor how severe your doctor is .
DIAGNOSIS:
DIAGNOSIS:
3.Body plethysmography: You’ll breathe in deeply for body plethysmography, which measures
how much air is in your lungs when you inhale. It also checks how much air stays in your lungs
after you breathe out as much as you can.
4. Chest X-ray.
5. Computed tomography.
6. Pulse oximetry.
7. Arterial blood gas test: This test measures the levels of gases like oxygen and carbon dioxide in
blood taken from one of your arteries.This test is used to check how well your lungs are able
to move oxygen into the blood and remove carbon dioxide from the blood.
REFERENCES :
◦ Dipiro
◦ Slideshares:
1. https://www.slideshare.net/mobile/draslam1/copd-aslam
2. https://images.app.goo.gl/byxxUjEtcicBd4Ld7
Wikipedia:
https://images.app.goo.gl/sSbm89Za5x4MSXoA7.
..THANK YOU..

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COPD.pptx

  • 1. COPD CHRONIC OBSTRUCTIVE PULMONARY DISEASE BY K.GOWRI PRIYA 19AB1T0011 PHARMD II
  • 2. Introduction: DEFINITION: COPD is defined as a disease state characterised by the presence of airflow obstruction due to chronic bronchitis or emphysema.The airflow obstruction is generally Progressively , may be accompanied by airway hyper reactivity & may be partially reversible. COPD is also known as chronic Obstructive lung disease (COLD), Chronic obstructive airway disease (COAD), Chronic airflow limitation(CAL), Chronic Obstructive Respiratory Disease (CORD). COPD refers to chronic bronchitis & Emphysema,a pair of 2 commonly co-existing diseases of the lungs in which the airways become narrowed.This leads to limitation of the airflow.
  • 3. AETIOLOGY: ◦ Cigarette Smoke. ◦ Genetics – Alpha 1 antitrypsin deficiency. ◦ Occupational exposure to chemicals. ◦ Ambient Air pollution. ◦ Sudden airway constriction in response to inhaled irritants. ◦ Bronchial hyper responsiveness.
  • 4. TYPES OF COPD: There are 2 types of COPD. They are: 1) Chronic bronchitis 2) Emphysema (1). CHRONIC BRONCHITIS: It is a chronic inflammation of the lower respiratory tract characterised by excessive mucous secretion , cough& dyspnea associated with recurrent infections of the lower respiratory tract. (Or) Chronic bronchitis is inflammation (swelling) and irritation of the bronchial tubes. These tubes are the airways that carry air to and from the air sacs in your lungs. The irritation of the tubes causes mucus to build up.
  • 5. TYPES OF COPD (2) EMPHYSEMA : It is a complex lung disease characterized by damage to the gas exchanging surfaces of the lungs (alveoli). (Or) A disorder affecting the alveoli (tiny air sacs) of the lungs. The transfer of oxygen and carbon dioxide in the lungs takes place in the walls of the alveoli. In emphysema, the alveoli become abnormally inflated, damaging their walls and making it harder to breathe.
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  • 7. RISK FACTORS: Risk factors for COPD include: • Exposure to tobacco smoke. The most significant risk factor for COPD is long-term cigarette smoking. The more years you smoke and the more packs you smoke, the greater your risk. Pipe smokers, cigar smokers and marijuana smokers also may be at risk, as well as people exposed to large amounts of secondhand smoke. • People with asthma. Asthma, a chronic inflammatory airway disease, may be a risk factor for developing COPD. The combination of asthma and smoking increases the risk of COPD even more. • Occupational exposure to dusts and chemicals. Long-term exposure to chemical fumes, vapors and dusts in the workplace can irritate and inflame your lungs. • Exposure to fumes from burning fuel. In the developing world, people exposed to fumes from burning fuel for cooking and heating in poorly ventilated homes are at higher risk of developing COPD. • Genetics. The uncommon genetic disorder alpha-1-antitrypsin deficiency is the cause of some cases of COPD. Other genetic factors likely make certain smokers more susceptible to the disease
  • 8. CAUSES OF AIRWAY OBSERVATION: Causes of airway obstruction include: • Emphysema: This lung disease causes destruction of the fragile walls and elastic fibers of the alveoli. Small airways collapse when you exhale, impairing airflow out of your lungs.
  • 9. TYPES OF EMPHYSEMA: In emphysema, the inner walls of the lungs’ air sacs (alveoli) are damaged, causing them to eventually rupture. This creates one larger air space instead of many small ones and reduces the surface area available for gas exchange. 1). Centrilobular emphysema : it is caused due to abnormal dilation or destruction of all respiratory bronchioles the central position of the acinus.It is commonly associated with cigarette smoking.
  • 10. TYPES OF EMPHYSEMA: 2). Panacinar Emphysema : It refers to enlargement or destruction of all parts of the acinar it is seen in alpha 1antitrpsin deficiency and in s.Panacinar emphysema : It refers to enlargement or destruction of all parts of the acinar it is seen in alpha 1antitrpsin deficiency and in smokers.
  • 11. TYPES OF EMPHYSEMA: 3). Paraseptal Emphysema:It usually involves the distal part of the secondary lobule the alveolar ducts are predominantly affected.
  • 12. PATHOPHYSIOLOGY: Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs. The latter represents the innate and adaptive immune responses to long term exposure to noxious particles and gases, particularly cigarette smoke.All cigarette smokers have some inflammation in their lungs, but those who develop COPD have an enhanced or abnormal response to inhaling toxic agents. This amplified response may result in mucous hypersecretion (chronic bronchitis), tissue destruction (emphysema), and disruption of normal repair and defence mechanisms causing small airway inflammation and fibrosis (bronchiolitis). Molecular mechanisms of COPD Pathogenesis. Chronic exposure to noxious stimuli like cigarette smoke produces differential effects on multiple lung cell types. The complexity of this interaction produces lung remodeling that is both pro-fibrotic in airways and matrix-degrading in the alveolar space.
  • 14. PATHOPHYSIOLOGY: ◦ These pathological changes result in increased resistance to airflow in the small conducting airways, increased compliance of the lungs, air trapping, and progressive airflow obstruction— all characteristic features of COPD. We have good understanding of the cellular and molecular mechanisms underlying the pathological changes found in COPD.
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  • 16. SYMPTOMS: ◦ COPD symptoms often don't appear until significant lung damage has occurred, and they usually worsen over time, particularly if smoking exposure continues. ◦ Signs and symptoms of COPD may include: ◦ • Shortness of breath, especially during physical activities ◦ • Wheezing ◦ • Chest tightness ◦ • A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or greenish ◦ • Frequent respiratory infections ◦ • Lack of energy ◦ • Unintended weight loss (in later stages) ◦ • Swelling in ankles, feet or legs.
  • 17. Clinical manifestations of chronic bronchitis : • Hypoxemia • Hypercapnia • Polycythemia • Cyanosis • Cor pulmonale Clinical manifestations of Emphysema: 1).Early stages 1. Dyspnea 2. Non productive cough 3. Diaphragm flattens 4. Barrel chest 5. Respiratory alkalosis 2). Later stages 1. Hypercapnea 2. Purse lip breathing 3. Underweight 4. Lung sounds diminished
  • 18. Your doctor will ask about your smoking history and listen to your lungs with a stethoscope. You may take tests, including: 1. Pulmonary function tests: This is a series of measurements of how much air your lungs can hold while breathing in and out. 2. Spirometry : The test measures two things : •The most air you can breathe out after inhaling deeply. The results will let you knowif you’re less able to breathe normally. •Exploratory ratio =FEV1/FVC. How much air you can exhale in 1 second. The score tells your doctor how severe your doctor is . DIAGNOSIS:
  • 19. DIAGNOSIS: 3.Body plethysmography: You’ll breathe in deeply for body plethysmography, which measures how much air is in your lungs when you inhale. It also checks how much air stays in your lungs after you breathe out as much as you can. 4. Chest X-ray. 5. Computed tomography. 6. Pulse oximetry. 7. Arterial blood gas test: This test measures the levels of gases like oxygen and carbon dioxide in blood taken from one of your arteries.This test is used to check how well your lungs are able to move oxygen into the blood and remove carbon dioxide from the blood.
  • 20. REFERENCES : ◦ Dipiro ◦ Slideshares: 1. https://www.slideshare.net/mobile/draslam1/copd-aslam 2. https://images.app.goo.gl/byxxUjEtcicBd4Ld7 Wikipedia: https://images.app.goo.gl/sSbm89Za5x4MSXoA7.