this presentation contains a detailed description about bronchitis ,its types, pathology,causes, treatment etc.

1. BY
SROTA DAWN.
M.PHARM [PHARMACOLOGY]
SUBJECT - PHARMACOLOGY -∏
VELS SCHOOL OF PHARMACEUTICAL SCIENCES
BRONCHITIS
[PATHOLOGY & TREATMENT]
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2.  Chronic obstructive pulmonary disease.
 Bronchitis, emphysema, and asthma may
present alone or in combination.
AsthmaBronchitis
Emphysema
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3. Description
 Characterized by presence of airflow
obstruction
 Caused by emphysema or chronic bronchitis
 Generally progressive
 May be accompanied by airway hyperreactivity
 May be partially reversible
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4. Emphysema
 Abnormal permanent enlargement of the air
space distal to the terminal bronchioles
 Accompanied by destruction of bronchioles
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5. Muscle contraction
Mucosal oedema
Sticky mucus
R2
R2
Bronchitis case
Normal
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7. COPD Causes
 Infection
 Major contributing factor to the
aggravation and progression of COPD
 Heredity
 -Antitrypsin (AAT) deficiency (produced
by liver and found in lungs); accounts for
< 1% of COPD cases
 Emphysema results from lysis of lung tissues by
proteolytic enzymes from neutrophils and macrophages
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8. TYPES OF BRONCHITIS:
CHRONIC
BRONCHITIS ACUTE
BRONCHITIS
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9. Chronic bronchitis
•Chronic bronchitis is
a chronic inflammation
of the bronchi (medium-size airways) in
the lungs.
• It is generally considered one of the two
forms of chronic obstructive pulmonary
disease (COPD), the other being emphysema.
•Chronic bronchitis It is defined clinically as a
persistent cough that produces sputum and
mucus, for at least three months per year in
two consecutive years.
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10. Signs and symptoms
Bronchitis may be indicated by –
 Cough (also known as a productive
cough, i.E. One that produces sputum),
 Shortness of breath and
 Wheezing.
Occasionally ,
chest pains, fever, and fatigue or malaise may also occur.
Mucus is often green or yellowish green and also may be
orange or pink, depending on the pathogen causing the
inflammation.
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11. Causes:
 Tobacco smoking is the most common cause.
Pneumoconiosis and long-term fume inhalation
are other causes.
Allergies can also cause mucus
hypersecretion, thus leading to symptoms
similar to asthma or bronchitis
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12. Pollution is a major cause of COPD
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13. Chronic Bronchitis Pathophysiology
Pathologic lung changes are:
 Hyperplasia of mucus-secreting glands
in trachea and bronchi
 Increase in goblet cells
 Disappearance of cilia
 Chronic inflammatory changes and narrowing
of small airways
 Altered function of alveolar macrophages
infections
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14. Chronic Bronchitis Pathophysiology
Chronic inflammation
Primary pathologic mechanism causing
changes
Narrow airway lumen and reduced
airflow
hyperplasia of mucus glands
Inflammatory swelling
Excess, thick mucus
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15. Chronic Bronchitis Pathophysiology
 Greater resistance to airflow increases
work of breathing
 Hypoxemia and hypercapnia develop more
frequently in chronic bronchitis than
emphysema
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16. Chronic Bronchitis Pathophysiology
 Bronchioles are clogged with mucus and
pose a physical barrier to ventilation
 Hypoxemia and hypercapnia , lack of
ventilation and O2 diffusion
 Tendency to hypoventilate and retain CO2
 Frequently patients require O2 both at rest
and during exercise
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17. Chronic Bronchitis Pathophysiology
 Cough is often ineffective to remove secretions
because the person cannot breathe deeply enough to
cause air flow distal to the secretions
 Bronchospasm frequently develops
More common with history of
smoking or asthma
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18. Chronic Bronchitis
Clinical Manifestations
 Earliest symptoms:
Frequent, productive cough during
winter
Frequent respiratory infections
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19. Chronic Bronchitis
Clinical Manifestations
 Bronchospasm at end of paroxysms of
coughing
 Cough
 History of smoking
 Normal weight or heavyset
 Ruddy (bluish-red) appearance d/t
 polycythemia (increased Hgb d/t chronic hypoxemia))
 cyanosis
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20. Chronic Bronchitis Clinical Manifestations
 Hypoxemia and hypercapnia
Results from hypoventilation and 
airway resistance + problems with
alveolar gas exchange
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21. Diagnosis:
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22. Diagnosis:
A variety of tests may be performed in patients
presenting with cough and shortness of breath:
•Pulmonary Function Tests (PFT)
(or spirometry)
•A chest X-ray
• chest radiography.
•A sputum sample showing neutrophil
granulocytes (inflammatory white blood cells)
and Check for pathogenic microorganisms such
as Streptococcus spp.
•A blood test would indicate inflammation
•High Resolution Computed Tomography (HRCT)
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23. COPD Complications
 Pulmonary hypertension (pulmonary vessel
constriction alveolar hypoxia & acidosis)
 Pneumonia
 Acute Respiratory Failure
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24. Acute bronchitis
Acute bronchitis is an inflammation of the large bronchi (medium-
size airways) in the lungs that is
Usually caused by viruses or bacteria and may last
several days or weeks.
Characteristic symptoms :
• cough,
• sputum (phlegm) production,
• shortness of breath
• wheezing related to the obstruction of the inflamed airways.
Diagnosis is by clinical examination and
sometimes microbiological examination of the phlegm.
Treatment
For acute bronchitis is typically symptomatic. As viruses cause
most cases of acute bronchitis, antibiotics should not be used unless
microscopic examination of gram-stained sputum reveals large numbers of
bacteria.
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25. Anti-inflammatory drugs: steroids
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26. Membrane
phospholipid
Arachidonic acid
Phospholipase A2
Leukotrienes:
B’constrictor
COX-I
PGs with gastric
protective effects
COX-II
PGs with inflammatory
effects
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27. Membrane
phospholipid
Arachidonic acid
Phospholipase A2
Leukotrienes
COX-I
PGs with gastric
protective effects
COX-II
PGs with inflammatory
effects
X
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28. Anti-inflammatory drugs: steroids
 Life-saving.
 Take at least 12 h to work: so start early in
severe cases.
 Systemic steriods: acute severe asthma.
 Inhaled steroids: maintenance
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29. Anti-inflammatory drugs: steroids
 Systemic steroid:
 intolerance
 ‘Cushingoid’ features
 Hypertension
 Salt and water retention
 Infection
 Topical steroid
 Hoarseness
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30. Anti-inflammatory drugs:
cromoglycate{mast cell stabilizer}
 Prevent release of histamine from mast cells
 By inhaler only.
 Useful maintenance therapy.
 No role in severe episodes.
 Few, if any, adverse effects.
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31. Anti-inflammatory drugs:
leukotriene receptor antagonists
Arachidonic acid
Leukotrienes
PGs with gastric
protective effects
PGs with
inflammatory
effectsx
Receptors
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32. • Leukotrienes cause capillary leakiness
and bronchoconstriction
• Used orally for maintenance therapy
(e.g. montelukast).
• Additive with inhaled steroids.
Anti-inflammatory drugs:
leukotriene receptor antagonists
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33. Bronchodilators
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34. Catecholamines, receptors and effects.
  receptors vasoconstrict
 1 receptors increase heart rate
 2 receptors vasodilate and bronchodliate
• Adrenaline , 1, 2.
• Noradrenaline , 1.
• Dobutamine () 1.
• Isoprenaline 1, 2.
• Salbutamol (1) 2.
HR,  BP, Bdilate
(HR),  BP
HR,  BP
HR, (? BP)
(HR), Bdilate
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35. 2-agonists.
 Salbutamol, terbutiline
 Inhalers (of various types).
 Maintenance:
 Regularly in more severe cases
 Acute severe asthma
 Tachycardia and tremor
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36. Aminophylline
 Is not a catecholamine, but has analgous effects.
 Narrow therapeutic range.
 Given by mouth or by IV infusion.
 Toxic:
 Fatal if injected too fast.
 Convulsions.
 Tachyarrhythmia
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37. Antimuscarinics
 Atropine is the classical antimuscarinic, and this
is b’dilator.
 Atropine: too many diverse effects.
 Ipratropium.
 By inhaler.
 Add to salbutamol.
 Dry mouth.
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