2. Bronchial asthma: definition
Clinical, physiological &pathological characteristics with the central
role of both chronic airway inflammation & increased airway hyper-
responsiveness.
Typical symptoms include wheeze, cough, chest tightness& dyspnoea
accompanied by the presence of airflow obstruction that is variable
over short periods of time, or is reversible with treatment.
3. Epidemiology:
The prevalence increased steadily over the last century
Current estimates: 300 million people world-wide& an additional 100
million persons will be diagnosed by 2025.
Although the development, course of disease& response to treatment
are influenced by genetic determinants, the rapid rise implies that
environmental factors are critically important in terms of its expression
like microbial exposure, diet, vitamins, breastfeeding, air pollution,
obesity, but no clear consensus has emerged
4. Pathophysiology:
Airway hyper-reactivity (AHR)—the tendency for airways to
contract too easily and too much in response to triggers that have
little or no effect in normal individuals—is integral to the diagnosis
of asthma.
5. Pathophysiology:
Atopy (produce IgE) Plays a central role.
Clear relationship between allergen exposure & sensitisation
(demonstration of skin prick reactivity or elevated serum IgE).
Inhalation of an allergen into the airway is followed by a two-
phase bronchoconstrictor response with both an early and a late-
phase response.
Common examples include house dust mites, pets(cats& dogs)
pests such as cockroaches, fungi.
6. Pathophysiology:
Influx of numerous inflammatory cells, the transformation
&participation of airway structural cells&the secretion of an
array of cytokines, chemokines& growth factors follow the initial
allergic response.
Smooth muscle hypertrophy& hyperplasia, thickening of the
basement membrane, mucous plugging& epithelial damage result.
With increasing severity & chronicity of the disease, remodelling
of the airway occurs, leading to fibrosis of the airway wall, fixed
narrowing of the airway&a reduced response to bronchodilators.
7. Pathophysiology:
Allergic mechanisms are also implicated in some cases of
occupational asthma
In aspirin-sensitive asthma, apirin inhibit the cyclo-oxygenase,
&shunting of arachidonic acid metabolism through the
lipoxygenase pathway, resulting in the production of
bronchconstrictor leukotrienes.
In exercise-induced asthma, hyperventilation results in water
/heat loss from the pericellular lining fluid of the respiratory
mucosa, which in turn triggers mediator release.
19. Pathophysiology:
COPD of 2 types chronic bronchitis & emphysema, but mostly
combined.
COPD has both pulmonary & systemic components.
There are changes in pulmonary & chest wall compliance because
the collapse of intrathoracic airways during expiration is
exacerbated, during exercise as the time available for expiration
shortens, resulting in dynamic hyperinflation.
Increased V/Q mismatch increases the dead space volume&wasted
ventilation.
20. Pathophysiology:
Flattening of the diaphragmatic muscles& an increasingly
horizontal alignment of the intercostal muscles place the
respiratory muscles at a mechanical disadvantage.
The work of breathing is therefore markedly increased, first on
exercise but, as the disease advances, at rest too.
Emphysema may be centriacinar, panacinar, periacinar& Bullae
form in some individuals&results in impaired gas exchange&
respiratory failure.
