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resp disorders pt.3
| Question | Answer |
|---|---|
| Obstructive lung disorders | asthma, chronic bronchitis, emphysema, cystic fibrosis, bronchiectasis |
| bronchiectasis | permanent widening and thickening of the airways (bronchi) |
| dyspnea | lack of O2 |
| What do obstructive lung disorders impair? | oxygenation and perfusion |
| What does increased work of breathing lead to? | increase in metabolic demand |
| worsening airway obstruction during exhalation | inflammation, loss of support for small airways, bronchoconstriction, mucus in airways |
| role of smooth muscles | broncoconstriction, bronchodilation |
| anatomic airway structure | worsening airway obstruction during exhalation, role of smooth muscles, resistance to airflow |
| mechanisms of airflow obstruction in COPD | bronchus obstructed by mucus, but with intact alveoli; bronchus with thickened wall and slightly damaged alveoli; narrow bronchus and heavily damaged alveoli |
| Pulmonary function tests (PFTs) uses | assessment of obstructive lung disorders |
| Pulmonary function tests types | spirometry, body plethysmography, nitrogen washout |
| tidal volume value | 500 mL |
| tidal volume | volume of air inhaled and exhaled during one cycle of normal quiet breathing |
| Inspiratory reserve volume (IRV) value | 3000 mL |
| Inspiratory reserve volume | max volume of air that can be inhaled after TV inhalation |
| inspiratory capacity volume | 3500mL |
| inspiratory capacity | max volume of air that can be inhaled after normal exhalation |
| expiratory reserve volume value | 1200 mL |
| expiratory reserve volume | max volume of air that can be exhaled after TV exhalation |
| vital capacity value | 4700 mL |
| vital capacity | max amount of air that can be exhaled in non forced manner after max inhalation |
| what is the most common obstructive condition? | asthma |
| asthma | chronic inflammatory disorder of airways, hyper reactive airways |
| Asthma is recurrent episodes of what? | reversible airway obstruction |
| Where is asthma greatest in? | industrialized countries |
| Asthma risk factors | genetics, obesity, exposure to allergens, irritants, tobacco smoke |
| How many people in the US have asthma? | over 28 million, about 1 in 12 |
| etiology of asthma | unknown |
| Asthma classification considerations | clinical presentation, precipitating factors or triggers, allergies |
| Asthma triggers | allergies, infections, exercise, medications |
| Asthma types | allergic asthma, recurrent asthma |
| allergic asthma (most common) | allergen causes type 1 hypersensitivity response |
| recurrent asthma | airways remodeled, bronchial smooth muscles hypertrophy, increasing capacity for bronchoconstriction |
| precipitating factors of asthma: allergens | classic type 1 hypersensitivity |
| precipitating factors of asthma: allergens examples | cockroach feces, dust mites, pollens, pet dander |
| precipitating factors of asthma: occupational stimuli | symptoms abate when individual is away from work |
| precipitating factors of asthma: occupational stimuli examples | organic and inorganic dusts, industrial chemicals, pharmaceutical agents |
| precipitating factors of asthma: infection | children under two years: respiratory syncytial virus older children: rhinoviruses, parainfluenza viruses |
| precipitating factors of asthma: exercise | 10-15 minutes of physical exertion, increased heat and water loss from bronchial mucosa |
| precipitating factors of asthma: medications | aspirin and non steroidal anti-inflammatory agents |
| precipitating factors of asthma: air pollution | ozone, sulfur dioxide, and nitrogen oxides |
| precipitating factors of asthma: strong emotions | vagal stimulation and acetylcholine release |
| What happens after a stimulus is detected during an acute episode of asthma? | chemical mediator release |
| What happens after a chemical mediator is released during an acute episode of asthma? | bronchospasm, inflammatory cell activation-> epithelial damage, edema, increased mucus production-> increased airway resistance, obstruction, and airflow limitation |
| asthma clinical manifestations | recurrent chest tightness, shortness of breath, wheezing, cough with or without production of thick sputum |
| clinical manifestations of severe asthma episodes | tachypnea and tachycardia |
| asthma severity classifications | mild intermittent asthma; mild, moderate, or severe persistent asthma |
| asthma diagnosis | medical history and physical examination, PFTs before and after bronchodilator use, challenge test, exhaled nitrogen oxide |
| asthma treatment | environmental control, bronchodilator, anti-inflammatory medications |
| chronic obstructive pulmonary disease | progressive airflow limitations that are not fully reversible- includes chronic bronchitis and emphysema |
| what is COPD linked to? | cigarette smoking |
| What percent of COPD is smoking accounted for? | 90% of COPD in industrialized countries |
| Onset of COPD | gradual onset with slowly progressive symptoms of dyspnea and shortness of breath (SOB) |
| COPD risk factors | direct and environmental tobacco smoke, genetics, occupational exposure, indoor air pollution, severe respiratory tract infections |
| COPD etiology | chronic airflow limitation due to abnormal inflammatory response to inhaled particles and gases in lung |
| GOLD 1: mild COPD | mild airflow limitation, possible chronic cough and sputum production, possible unawareness of individual that lung function is abnormal |
| GOLD 2: moderate COPD | worsening airflow limitations, SOB on exertion, possible chronic cough and sputum production, chronic respiratory symptoms lead to person seeking care |
| GOLD 3: severe COPD | further worsening of airflow limitations, greater SOB; reduced exercise capacity, fatigue, and repeated exacerbations, affect on patient's quality of life |
| GOLD 4: very severe COPD | severe airflow limitations plus chronic respiratory failure |
| COPD pathophysiology | airway obstruction results from fixed airways that have increased resistance, slowing the rate of airflow, hypercapnia, hyperinflation |
| What slows the rate of airflow in COPD? | chronic inflammation, structural remodeling of lung tissue, alterations in vascular structure, destruction of pulmonary structures |
| hypercapnia | excess of carbon dioxide in the blood |
| Pathogenesis of COPD- what happens when tobacco smoke or air pollution enter lungs? | continual bronchial irritation and inflammation, breakdown of elastin in connective tissue of lungs |
| Pathogenesis of COPD- what happens when there is an a1-antitrypsin deficiency? | breakdown of elastin in connective tissue of lungs |
| pathogenesis of COPD- what happens after continual bronchial irritations and inflammation? | chronic bronchitis- bronchial edema, hyper secretion of mucus, chronic cough, bronchospasm |
| pathogenesis of COPD- what happens after the breakdown of elastin in connective tissue of lungs? | emphysema- destruction of alveolar septa, airway instability |
| pathogenesis of COPD- what happens after chronic bronchitis and emphysema? | airway obstruction, air trapping, dyspnea, frequent infections-> abnormal ventilation-perfusion ratio, hypoxemia, hypoventilation, cor pulmonale |
Created by:
camrynfoster