Altered Respiratory Functions Part 3

Altered Respiratory Functions (Part 3)

• Objectives: Students should describe the triggers, pathophysiology, and manifestations of acute asthma attacks. They should also describe COPD pathogenesis and manifestations, and differentiate between chronic bronchitis and emphysema causes and manifestations.

Obstructive Lung Diseases

• Included in this category are Asthma and COPD.

Obstructive Airway Disorders

• Caused by increased resistance to airflow.
• Parasympathetic stimulation (cholinergic receptors and vagus nerve) leads to bronchoconstriction.
• Sympathetic stimulation (B2-adrenergic receptors) produces bronchodilation.
• Bronchial smooth muscle reacts to inflammatory mediators (histamine, cytokines) causing bronchoconstriction.

Asthma: Definition

• Characterized by periodic episodes of severe, but reversible, bronchial obstruction in persons with hypersensitive or hyperresponsive airways.
• Frequent acute asthma attacks can lead to irreversible lung damage and chronic asthma (COPD).

Etiology/Precipitating Factors

• Exact cause unknown.
• Asthma triggers induce hypersensitivity reactions and inflammatory responses.
• Common triggers include allergens (pollen, mold, pets, dust mites, cockroach, animal dander, fungus), irritants (cigarette smoke, cleaning chemicals, fragrances, cold air), and exercise.

Bronchial Asthma: Types

• Extrinsic (Atopic) Asthma: Initiated by type 1 hypersensitivity reactions from exposure to extrinsic antigens or allergens. Most common in childhood and adolescence. Common allergens include house dust mite allergens, cockroach, pollen, and animal dander.
• Intrinsic (Nonatopic) Asthma: Includes hyperventilation, cold air, exercise, emotional upset, aspirin and other NSAIDs, and gastroesophageal reflux. Exercise-induced asthma may result from heat and water loss from the tracheobronchial tree, which impairs warming and humidification. Inhaled irritants (such as tobacco smoke and strong odors) can induce asthma via irritant receptors. Emotional factors trigger bronchospasms due to the vagal pathway, increasing responsiveness to other triggers. Reflux of gastric secretions act as a bronchospastic trigger.

Pathophysiology (Asthma)

• Early-phase (10-20 minutes): Antigen exposure activates mast cells releasing various mediators including histamine. This leads to increased mucus production, bronchoconstriction, and vascular permeability, causing edema.
• Late-phase (6-24 hours): Inflammatory cells infiltrate the airways; further bronchospasm and inflammation occur, with more mucus production and epithelial injury.

Pathophysiology (Acute Episode)

• Edema of mucous membrane: Initial swelling impacts airways.
• Mucus plug: Accumulation of mucus obstructs airflow.
• Bronchospasm (muscle contraction): The bronchiole muscles contract, reducing the lumen of the airways.
• Obstructive bronchiole: The combination of mucus plug and bronchospasm obstructs the bronchioles significantly reducing airflow.

Asthma: Summary

• Inflammatory mediators initiate airway inflammation, edema (especially of mucous lining), bronchospasm, and impaired secretion clearance.

Clinical Manifestations (Asthma)

• Wheezing, breathlessness, chest tightness.
• Excessive sputum production and coughing.
• Using accessory muscles, fatigue.
• Anxiety, dyspnea, tachypnea, hyperventilation, leading to initial respiratory alkalosis.
• Respiratory acidosis may develop later due to air trapping.
• Hypoxia (low oxygen).

Asthma: Treatment

• General measures: Skin tests for allergic reactions, avoidance of triggers, good ventilation, and use of maintenance inhalers/drugs (swimming and walking).
• Measures for acute attacks: Controlled breathing techniques, inhalers (bronchodilators), and glucocorticoids (beclomethasone).

COPD: Definition

• Group of chronic respiratory disorders.
• Causes irreversible and progressive lung damage
• Debilitating conditions affecting work ability.
• May result in cor pulmonale.
• Respiratory failure possible.

COPD: Components

• Asthma
• Emphysema
• Chronic bronchitis

Emphysema: Definition

• Irreversible enlargement of air spaces beyond terminal bronchioles (alveoli), resulting in alveolar wall destruction and airflow obstruction.
• Loss of surface area for gas exchange.
• Loss of pulmonary capillaries.
• Loss of elastic fibers.
• Alteration of ventilation-perfusion ratio.
• Decreased support for other structures.

Emphysema: Etiology

• Smoking is the most common cause (80-90% of cases).
• Occupational exposure to industrial pollutants accounts for about 20%.
• Genetic factor: Alpha-1-antitrypsin (AAT) deficiency.

Emphysema: Pathophysiology

• Smoking increases elastase release in the lungs.
• When a-antitrypsin levels are low, it's unable to neutralize elastase, which damages lung tissues.
• Damaged elastic fibers prevent lung recoil, resulting in airway collapse and air trapping.

Emphysema: Pathophysiology (Air Trapping)

• Impaired expiratory recoil.
• Air trapping and increased residual volume.
• Overinflation of the lungs (barrel chest).
• Fixation of ribs in a respiratory position, increasing the anterior-posterior diameter of the thorax (barrel chest).
• Flattened diaphragm (on radiographs).

Emphysema: Clinical Manifestations

• Insidious onset.
• Dyspnea.
• Prolonged expiratory phase.
• Hyperinflation (barrel chest).
• Anorexia, fatigue leading to weight loss.

Emphysema: Treatment

• Smoking cessation is essential.
• Oxygen therapy.
• Appropriate breathing techniques (e.g., pursed-lip breathing).

Chronic Bronchitis: Definition

• Airway obstruction in major and small airways.
• Chronic irritation from smoking or recurrent infections.
• Hypertrophy of submucosal glands in the trachea and bronchi.

Chronic Bronchitis: Etiology

• Cigarette smoking.
• Living in urban or industrial areas.
• Exposure to environmental pollutants.

Chronic Bronchitis: Pathophysiology

• Chronic irritation leads to hypertrophy (enlargement) of submucosal glands.
• Increased mucus production.
• Obstruction of airways by mucus plugs.
• Reduced cilia action (impaired clearance), enabling microorganisms to accumulate.

Chronic Bronchitis: Clinical Manifestations

• Chronic productive cough (purulent sputum).
• Dyspnea.
• Wheezing and crackles on auscultation.
• Hypoxemia, hypercapnia (increased carbon dioxide), and cyanosis.

Chronic Bronchitis: Treatment

• Smoking cessation.
• Bronchodilator therapy.
• Steroid antiinflammatory drugs.
• Supplemental oxygen therapy.

Nursing Considerations

• Urge patients to stop smoking
• Encourage avoidance of respiratory irritants.
• Review the bronchodilators and antibiotics patients are using.

This quiz focuses on the triggers, pathophysiology, and manifestations of acute asthma attacks, as well as the pathogenesis and features of COPD. Students will also distinguish between chronic bronchitis and emphysema, understanding their causes and effects. Prepare to deepen your knowledge of obstructive lung diseases.