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Pathophysiology asthma.

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Asthma & COPD.

Asthma & COPD.

Published in: Health & Medicine

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  • 1. OBSTRUCTIVE PULMONARY DISEASES: BRONCHIAL ASTHMA & COPD Dr.Mohamed Shekhani.
  • 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.
  • 8. COPD
  • 9. 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.
  • 10. 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.