The document discusses chronic bronchitis, emphysema, and pulmonary hypertension. It defines each condition and describes their causes, pathophysiology, morphology, management, complications, symptoms, and methods of investigation including spirometry and chest x-rays. Chronic bronchitis involves inflammation of the bronchi due to smoking or air pollution. Emphysema is the permanent enlargement of airspaces due to an imbalance of proteases and antioxidants from smoking. Pulmonary hypertension is high blood pressure in the lungs secondary to lung damage from these conditions.

1. Free syria
RAHEEF ALATASSI

2. objectives
 chronic bronchitis :
 definition
 causes
 path physiology
 morphology
 mechanism of obstruction
 management
 complication
 S/S
 Investigation
 Emphysema:
 definition
 Causes
 path physiology
 morphology
 types
 management
 complication
 S/S
 Investigation
 Pulmonary hypertension:
 Definition

3. CHRONIC BRONCHITIS

4. Definition
 It is defined as a persistent productive
cough for at least 3 consecutive months in
at least 2 consecutive years
forms features
Simple chronic bronchitis the productive cough raises
mucoid sputum, but airflow is not
obstructed
Chronic asthmatic bronchitis hyper-responsive airways with
intermittent bronchospasm and
wheezing
Chronic obstructive bronchitis develops chronic outflow
obstruction
Associated with emphysema

5. Causes

6. Pathogenesis of Chronic Bronchitis
Pathogenesis of
Chronic Bronchitis mucous gland hyperplasia,
Cigarette smoking or other
air pollutants lead to:
 1-Hypertrophy and hyper
secretion of bronchial
mucous glands
 2-Metaplastic formation
of goblet cells
 3-Infiltration by CD+8
lymphocytes
,macrophages and
neutrophils

7. morphology
 The trachea
in the mid-
upper field is
hyperemic
 the
bifurcation &
bronchi
contain
mucopurulent
exudate
secretion.

8.  enlargement of the mucus-secreting
glands

9. management
 Stop smoking > inhaled bronchodilator
(anticholinergic agonist or b2 agonist) >
combination > glucocorticosteroid > oxygen.

10. Complications:
 Pulmonary hypertension and cardiac failure
 Recurrent infections
 Respiratory failure
S/S :
 cough , sputum ,frequent infections ,
intermittent dyspnea, wheeze.
 Some patients develop significant COPD
with outflow obstruction: hypercapnia,
hypoxemia, cyanosis

11. The severity of COPD also depends on the severity of dyspnea and exercise limitation. These and
Investigation
 Spirometry
Severity of COPD (GOLD scale) FEV1 % predicted
Mild ≥80
Moderate 50–79
Severe 30–49
<30 or chronic respiratory failure
Very severe
symptoms
 CXR > hyperinflation
 FBC > polycythemia
 ABG > hypoxemia or hypercapnia

12. Spirometry

13. EMPHYSEMA

14. definition
• It is permanent enlargement of air spaces
distal to terminal bronchioles, accompanied
by destruction of their walls.
• not associate with fibrosis
Causes:
Smoking
Deficinecy of a1 antitrypsin

15. path physiology

16. Pathogenesis of Emphysema
Tobacco smoke
Emphysema arises as a consequence of
two imbalances: free radical
Protease-antiprotease imbalance
Oxidant-antioxidant imbalance
INCRESE elastase
The destructive effect of protease in
subjects with low antiprotease activity
leads to emphysema
free radical
Protease release
Free radical → deplete the lung
antioxidant mechanisms → tissue
damage

17. morphology
 The external surfaces of the upper lobes
of both the right and left lungs have large
bullae.
 Distal type.
 bullae
Cyst
more than
1 cm.

18.  the permanent enlargement of the airspace,
accompanied by destruction of the septa

19. types
type features
It involve the central or proximal parts of the acini
Centriacinar The lesions are more common and severe in the upper
lobes
This type is seen as a result of cigarette smoking
It occurs more commonly in the lower lung zones
Panacinar The type of emphysema occurs in α1-antitrypsin
deficiency
 The distal part of the acinus is involved
Distal Acinar  It is seen adjacent to the pleura, along the lobular
margins,scarring.
 Cystlike structures can be formed (bullae)
The acinus is irregularly involved
Irregular It is associated with scarring
Clinically asymptomatic
The most common form of emphysema

21. Management & Investigation
The same treatment &
Investigation as the chronic
bronchitis

22. Pulmonary Hypertension in COPD
Chronic hypoxia
Pulmonary vasoconstriction
Muscularization
Pulmonary hypertension Intimal
hyperplasia
Fibrosis
Cor pulmonale Obliteration
Edema
Death

23. complication
I. Pulmonary hypertension;
 hypoxia-induced pulmonary vascular spasm
 loss of capillary surface area due to alveolar wall
destruction
II. Right side heart failure
III. Respiratory failure

24. S/S
 Patients present with dyspnea, and
abnormal pulmonary function tests
Patients with no bronchitis
Patients with underlying
chronic bronchitis They have more severe
dyspnea and
They have less dyspnea hyperventilation
and retain more CO2
 They are always hypoxic  They have normal gas
and cyanotic (blue exchange and adequate
bloaters) oxygenation of
hemoglobin (pink puffers)

25. Pulmonary hypertension:
 The pulmonary circulation is normally one of
low resistance, with pulmonary blood
pressures being only about one-eighth of
systemic pressure. Pulmonary hypertension
(when mean pulmonary pressures reach one-
fourth or more of systemic levels) is most
often secondary to a decrease in the cross-
sectional area of the pulmonary vascular bed,
or to increased pulmonary vascular blood
flow

26. morphology
 A, Gross photograph of
atheroma formation, a
finding usually limited to
large vessels.
 B, Marked medial
hypertrophy.
 C, Plexogenic lesion
characteristic of advanced
pulmonary hypertension
seen in small arteries.