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.
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
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.
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
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
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
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.
A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry. To help identify individuals earlier in the course of disease, spirometry should be performed for patients who have chronic cough and sputum production even if they do not have dyspnea. Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to spirometry.
air spaces distal to terminal bronchioles is (acini) respiratory bronchiole , alveolar duct , alveoli
Hypoxia in lung is special will induce pulmonary vasoconstriction that will elevate pulmonary hypertension, pressure overload right side heart failure