Asthma

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Etiopathagensis of Asthma Hatlan

Transcript of Asthma

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Etiopathagensis of Asthma

Hatlan

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Objectives • Epidemiology • Etiology• Symptoms • Types• Pathogenesis

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Epidemiology • 235 million people worldwide are affected by

asthma (2011). by 2025 > 100 million• 250,000 people die per year from the disease• Asthma is among the most common chronic

illnesses in Saudi Arabia• Female > Male• Saudi Arabia 24%,Qatar 19.8%,Kuwait

16.8%,UAE 13% in the (NME 2013)

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Etiology

• Hereditary • Environmental allergens.• Obesity• Exercise• Smoke• Drugs: NSAID• Viral respiratory tract infections• Gastroesophageal reflux disease• Occupational exposure• Emotional factors or stress

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Symptoms

• Coughing from asthma often is worse at night or early in the morning, making it hard to sleep.

• Wheezing. Wheezing is a whistling or squeaky sound that occurs when you breathe.

• Chest tightness. • Shortness of breath.

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Types of Asthma 1-Allergic or extrinsicAllergic asthma is a result of an antigen\antibody reaction on

mast cells in the respiratory tract. This reaction causes the release of inflammatory mediators from mast cells which elicit the clinical response associated with an asthma attack.

2-Intrinsic or idiosyncraticIdiosyncratic asthma is a result of neurological imbalances in

the autonomic nervous system (ANS) in which the alpha and beta adrenergic as well as the cholinergic sites of the ANS are not properly coordinated.

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Comparison

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Pathogenesis of Asthma • A triad of :

• Airway inflammation• Intermittent airflow

obstruction• Bronchial hyperresponsiveness

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Airway inflammation

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Airflow obstruction

• Airflow obstruction can be caused by a variety of changes, including :

1. acute bronchoconstriction, 2. airway edema, 3. chronic mucous plug formation,4. airway remodeling.

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Airflow obstruction

• Airway obstruction causes • increased resistance to airflow and decreased

expiratory flow rates and this lead to a decreased ability to expel air and may result in hyperinflation.

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Bronchial hyperresponsiveness

• Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation.

• This eventually will lead to hypoxia.• In the late stages due to increase breathing and

COP metabolic acidosis occurs and very late respiratory acidosis.

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