MS. SHIVANGI MISTRY
M.PHARM (PHARMACOLOGY)
ASSISTANT PROFESSOR
BHAGWAN MAHAVIR COLLEGE OF PHARMACY
Date : 13-8-20 time : 10 -11 pm
CONTENT
Definition
Difference between asthma and COPD
Causes, incidence and risk factor
Patho-physiology
Symptoms
Complication
Diagnosis
Prevention
Treatment
Pro-diagnosis 2
Definition
• COPD :
o Chronic obstructive airways diseases (COAD)
o Chronic obstructive lung diseases (COLD)
o Chronic bronchitis
o Emphysema
• Definition :
o Makes difficult to breathe.
o Air flow limitation is usually progressive & is associated
with abnormal inflammatory response of lungs to noxious
particles or gases, primarily caused by cigarette smoking.
3
• Mainly in two form:
1. Chronic bronchitis :
 Chronic bronchitis is defined clinically as a daily cough
with production of sputum at least 3 month per year for 2
or more consecutive year.
 It involves inflammation and swelling of the lining of the
air way that leads to narrowing and obstruction of the air
way.
 The inflammation also stimulate production of mucus
which can cause further obstruction of the airway.
4
5
2. Emphysema :
 It is permanent enlargement of the alveoli due to
destruction of the wall between alveoli which leads to
reduce the elasticity of the lungs over all.
 Loss of elasticity leads to collapse of the bronchioles,
obstructing air flow out of the alveoli. Air become trapped
to the alveoli and reduce the ability of the lungs to shrink
during exhalation .
6
Difference between asthma and COPD
7
8
Causes, incidence and risk factor
• Causes and incidense :
o Smoking is leading factor.
o In rare cases, non-smokers who lack a protein called alpha-1
antitrypsin can develop emphysema.
• Risk factors :
o Host factors :
 Genetic factor
 Sex
 Air way hypereactivity,
 Immunoglobulin E
 Asthma 9
o Exposures :
 Smoking
 Socioeconomic status
 Occupation
 Enviromental pollution
 Perinatal events and childhood illness
 Recurrent bronchopulmonary infection
 Diet
o Other risk factor :
 Exposure to certain gases or fumes in the workplace
 Exposure to heavy amt. of secondhand smoke & pollution
 Frequent use of cooking fire without proper ventilation 10
11
Pathophysiology
1) Mucous hypersecretion & cilliary dysfunction:
 Stimulated secretion from anlarged mucous gland &
squamous metaplasia of epithelial cells.
2) Airflow limitation & hyperinflation :
 The major site of airflow limitation is in smaller
conducting airways <2 mm in diameter & is mainly due to
airway remodeling (fibrosis & narrowing).
 Other factors that also contribute include loss of elastic
recoil (due to destruction of alveolar walls), destruction of
alveolar support (alveolar attachment), accumulation of
inflammatory cells, mucous & plasma exdates in bronchi,
& smooth muscle contactn & dynamic hyperinflamation
during exercise. 12
3) Gas exchange abnormalities :
 Abnormal distribution of ventilation perfusion ratios (due
to anatomical alternations)
 Abnormal diffusing capacity of carbon dioxide/ litre of
alveolar vol. correlates well with severity of emphysema.
4) Pulmonary hypertension:
 Factors include vasoconstriction (hypoxic origin),
endothelial dysfunction, remodelling of pulmonary arteries
& destruction of pulmonary capillary bed.
 This combination of events may eventually lead to right
ventricular hypertrophy & dysfunction. 13
5) Systemic effects:
 Associated with extra pulmonary effects, including
systemic inflammation & skeletal muscle wasting.
 Contributes to limit exercise capacity of these patients & to
worsen prognosis, independent of their pulmonary
function.
14
 Symptoms :
• Cough with or without mucus
• Fatigue
• Many respiratory infection
• Shortness of breath (dyspnea) that gets worse with
mild activity
• Trouble catching one’s breath
• Wheezing
15
Common signs are
• Tachypnea a rapid breathing rate
• Wheezing sounds or crackles in the lungs heard through a
stethoscope
• Breathing out taking a longer time than breathing in
• Enlargement of the chest, particularly the front-to-back
distance (hyperaeration)
• breathing through pursed lips
• Increased anteroposterior to lateral ratio of the chest (i.e.
barrel chest)
16
Complication
• Irregular heart beat (arrhythmia)
• Need for breathing machine & oxygen therapy
• Right side heart failure
• Pneumonia
• Pneumothorax
• Severe wt. loss & malnutrition
• Thinning of the bones (osteoporosis)
17
Diagnosis
• Medical History
• Physical examination finds enlarged chest cavity and
wheezing.
• Blood Test
• A hematocrit value of more than 52% in males and more
than 47% in female indicates disease.
• Measure the alpha1-antitrypsin (AAT), the AAT level is low.
• Sputum for culture and microscopic examination mucoid
sputum .
• The pathogens Streptococcus pneumoniae and Haemophilus
influenzae.
18
Prevention
• Not smoking prevents most COPD. Medicines are also
available to help kick the smoking habit.
Treatment :
• Medications used to treat COPD include :
 Inhalers (bronchodilator), to open the air ways, such as
ipratropium, salmeterol, formoterol or albuterol.
 Inhaled steroid to reduce lung inflamation
 Anti-inflammatory medications such as mentelukast and
rotlimulast are sometimes uesd.
19
• In severe cases or during flare-ups, following can be used:
 Steriods by oral or IV
 Bronchodilators through a nebulizer
 Oxygen therapy
 Assistance during breathing (through a mask or endotracho
tube)
20
Pro-diagnosis
• COPD is long-term (chronic) illness.
• Patients with severe COPD will be short of breath with most
activities and will be admitted to the hospital more often.
• These patients should consult with their doctors about
breathing method, and other life care treatment methods.
21
22

Chronic obstructive airways diseases

  • 1.
    MS. SHIVANGI MISTRY M.PHARM(PHARMACOLOGY) ASSISTANT PROFESSOR BHAGWAN MAHAVIR COLLEGE OF PHARMACY Date : 13-8-20 time : 10 -11 pm
  • 2.
    CONTENT Definition Difference between asthmaand COPD Causes, incidence and risk factor Patho-physiology Symptoms Complication Diagnosis Prevention Treatment Pro-diagnosis 2
  • 3.
    Definition • COPD : oChronic obstructive airways diseases (COAD) o Chronic obstructive lung diseases (COLD) o Chronic bronchitis o Emphysema • Definition : o Makes difficult to breathe. o Air flow limitation is usually progressive & is associated with abnormal inflammatory response of lungs to noxious particles or gases, primarily caused by cigarette smoking. 3
  • 4.
    • Mainly intwo form: 1. Chronic bronchitis :  Chronic bronchitis is defined clinically as a daily cough with production of sputum at least 3 month per year for 2 or more consecutive year.  It involves inflammation and swelling of the lining of the air way that leads to narrowing and obstruction of the air way.  The inflammation also stimulate production of mucus which can cause further obstruction of the airway. 4
  • 5.
  • 6.
    2. Emphysema : It is permanent enlargement of the alveoli due to destruction of the wall between alveoli which leads to reduce the elasticity of the lungs over all.  Loss of elasticity leads to collapse of the bronchioles, obstructing air flow out of the alveoli. Air become trapped to the alveoli and reduce the ability of the lungs to shrink during exhalation . 6
  • 7.
  • 8.
  • 9.
    Causes, incidence andrisk factor • Causes and incidense : o Smoking is leading factor. o In rare cases, non-smokers who lack a protein called alpha-1 antitrypsin can develop emphysema. • Risk factors : o Host factors :  Genetic factor  Sex  Air way hypereactivity,  Immunoglobulin E  Asthma 9
  • 10.
    o Exposures : Smoking  Socioeconomic status  Occupation  Enviromental pollution  Perinatal events and childhood illness  Recurrent bronchopulmonary infection  Diet o Other risk factor :  Exposure to certain gases or fumes in the workplace  Exposure to heavy amt. of secondhand smoke & pollution  Frequent use of cooking fire without proper ventilation 10
  • 11.
  • 12.
    Pathophysiology 1) Mucous hypersecretion& cilliary dysfunction:  Stimulated secretion from anlarged mucous gland & squamous metaplasia of epithelial cells. 2) Airflow limitation & hyperinflation :  The major site of airflow limitation is in smaller conducting airways <2 mm in diameter & is mainly due to airway remodeling (fibrosis & narrowing).  Other factors that also contribute include loss of elastic recoil (due to destruction of alveolar walls), destruction of alveolar support (alveolar attachment), accumulation of inflammatory cells, mucous & plasma exdates in bronchi, & smooth muscle contactn & dynamic hyperinflamation during exercise. 12
  • 13.
    3) Gas exchangeabnormalities :  Abnormal distribution of ventilation perfusion ratios (due to anatomical alternations)  Abnormal diffusing capacity of carbon dioxide/ litre of alveolar vol. correlates well with severity of emphysema. 4) Pulmonary hypertension:  Factors include vasoconstriction (hypoxic origin), endothelial dysfunction, remodelling of pulmonary arteries & destruction of pulmonary capillary bed.  This combination of events may eventually lead to right ventricular hypertrophy & dysfunction. 13
  • 14.
    5) Systemic effects: Associated with extra pulmonary effects, including systemic inflammation & skeletal muscle wasting.  Contributes to limit exercise capacity of these patients & to worsen prognosis, independent of their pulmonary function. 14
  • 15.
     Symptoms : •Cough with or without mucus • Fatigue • Many respiratory infection • Shortness of breath (dyspnea) that gets worse with mild activity • Trouble catching one’s breath • Wheezing 15
  • 16.
    Common signs are •Tachypnea a rapid breathing rate • Wheezing sounds or crackles in the lungs heard through a stethoscope • Breathing out taking a longer time than breathing in • Enlargement of the chest, particularly the front-to-back distance (hyperaeration) • breathing through pursed lips • Increased anteroposterior to lateral ratio of the chest (i.e. barrel chest) 16
  • 17.
    Complication • Irregular heartbeat (arrhythmia) • Need for breathing machine & oxygen therapy • Right side heart failure • Pneumonia • Pneumothorax • Severe wt. loss & malnutrition • Thinning of the bones (osteoporosis) 17
  • 18.
    Diagnosis • Medical History •Physical examination finds enlarged chest cavity and wheezing. • Blood Test • A hematocrit value of more than 52% in males and more than 47% in female indicates disease. • Measure the alpha1-antitrypsin (AAT), the AAT level is low. • Sputum for culture and microscopic examination mucoid sputum . • The pathogens Streptococcus pneumoniae and Haemophilus influenzae. 18
  • 19.
    Prevention • Not smokingprevents most COPD. Medicines are also available to help kick the smoking habit. Treatment : • Medications used to treat COPD include :  Inhalers (bronchodilator), to open the air ways, such as ipratropium, salmeterol, formoterol or albuterol.  Inhaled steroid to reduce lung inflamation  Anti-inflammatory medications such as mentelukast and rotlimulast are sometimes uesd. 19
  • 20.
    • In severecases or during flare-ups, following can be used:  Steriods by oral or IV  Bronchodilators through a nebulizer  Oxygen therapy  Assistance during breathing (through a mask or endotracho tube) 20
  • 21.
    Pro-diagnosis • COPD islong-term (chronic) illness. • Patients with severe COPD will be short of breath with most activities and will be admitted to the hospital more often. • These patients should consult with their doctors about breathing method, and other life care treatment methods. 21
  • 22.