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Obstructive Pulmonar
Stack #166921
| Question | Answer |
|---|---|
| This class diseases results from the narrowing or obstruction of the tracheobronchial tree or from destruction of the pulmonary parenchyma. | Obstructive |
| Obstructive lung disease results in _____________ compliance of the lungs but a ______ elastic recoil | increased, decreased |
| clinical disorder characterized by excessive mucous secretion within the bronchial tree than cannot be explained by either a specific infection or by infiltrative disease. | Chronic bronchitis |
| clinically defined as a chronic cough with sputum production for at least three months of the year in at least two consecutive years. | Chronic bronchitis |
| major cause of chronic bronchitis is | cigarette smoking |
| Does air pollution and occupational irritants may also play a role in chronic brochitis? | yes |
| major pathophysiologic disruption in chronic bronchitis is | large airway obstruction |
| As a defense mechanism against chronic irritation of the tracheobronchial mucosa by cigarette smoke and/or other environmental pollutants, there is _______ and __________of the submucosal mucous glands in the large airways | hypertrophy, hyperplasia |
| Squamous ________&_________ of the surface epithelium may also be present, with chronic bronchitis | metaplasia, dysplasia |
| Goblet cell metaplasia of small bronchi and bronchioles also contributes to what 3 problems? | the excessive mucus production, decreases the number of normal ciliated, and predisposes to obstruction of these airways by mucous plugs. |
| Is air generally drawn into the aveoli with chroic bronchitis? | Yes |
| On expiration, with chronic bronchitis, what occurs? | the bronchioles collapse around the mucous plugs, air is trapped in the distal airways. |
| What is the pathophysiologic outcome with chronic bronchitis | fibrosis (bronchiolitis fibrosa obliterans) of the bronchiolar walls. |
| Are blood vessels affected by chronic bronchitis? | no |
| blood vessels are not significantly affected by chronic bronchitis, is a ventilation/perfusion mismatch. | yes |
| Why are individuals with chronic bronchitis cyanotic? | a greater proportion of their reduced hemoglobin is not converted to oxyhemoglobin as it passes through the lungs. |
| What will ABG's of chronic bronchitis client show? | Blood gases generally reveal a chronic hypoxemia |
| What does the chronic hypoxemia state in the chronic bronchitis client induce? | polycythemia,resulting in an acidotic state. |
| Will hypercapnia icrease acidotic state? | yes |
| With Chronic Bronchitis,acidosis promotes | pulmonary vasoconstriction |
| With Chronic Bronchcitis, the pulmonary vasoconstriction will do what to the v/q mispatch? | correct the V/Q mismatch (and improve pO2) by decreasing the perfusion |
| Pulmonary constriction, resulting in temporary correction of v/q mismatichc, will over time, will result in | pulmonary hypertension with ensuing right heart failure. |
| Chest x-rays will be normal or abnormal with chronic bronchitis? | Chest x-rays may be normal in appearance but, with bronchography, bronchial pits or diverticula representing the enlarged bronchial gland ducts are pathognomonic. |
| bronchography, bronchial pits or diverticula will show what with chronic bronchitis? | enlarged bronchial gland ducts are pathognomonic. |
| Complications of what type of obstructive disease. Repeated infections, right-sided heart failure, peptic ulcers, and respiratory failure are the major complications. | chronic bronchitis |
| This is defined as an abnormal, permanent, destructive lesion of the pulmonary parenchyma which leads to an increase in the size and volume of the air spaces distal to the terminal bronchiole. | EMPHYSEMA |
| The major pathophysiologic disruption of emphysema is | distal airway tissue destruction with resultant loss of elastic recoil |
| When do patients with emphysema have difficulty moving air? | expiration |
| due to a loss of the tethering effect of intact alveoli on the distal airways,with emphysema, they tend to | collapse upon themselves during expiration and trap air behind. |
| This pattern of emphysema is characterized by destructive changes primarily to the respiratory bronchioles. | Centrilobular |
| Type of emphysema, most striking in the upper lobes, it is seen most frequently in cigarette smokers | centrilobular |
| Centrilobular emphysema is frequently associated wtih chronic bronchitis in what type of clients? | smokers |
| Centrilobular emphysema, Both macrophage and neutrophilic proteases (elastase, etc) are released and unless they are inactivated by antiproteases such as alpha-1-antitrypsin, proteolytic digestion of the | alveolar walls will ensue. |
| Centrilobular emphysema, macrophages and neutrophilic proteases need to be inactivated by what? | antiproteases such as alpha-1-antitrypsin, |
| cigarette smoke also acts to directly inactivate the | protective alpha-1-antitrypsin. |
| Centrilobular emphysema, what are free radicals released by? | neutrophils |
| Type of emphysema, Most frequently seen in the lower lobes this pattern is characterized by uniform involvement of the acinus and is seen in patients with inherited or acquired alpha-1-antitrypsin deficiency, especially if they also smoke. | Panlobular |
| Type of emphysema this pattern is characterized by uniform involvement of the acinus and is seen in patients with inherited or acquired alpha-1-antitrypsin deficiency, especially if they also smoke. | Panlobular |
| What type of obstructive disease? CLINICAL - Patients usually present with a history of progressive dyspnea and often weight loss due to the increased work involved in respiration. | Emphysema |
| Type of obstructive disorder, The diameter of the chest is increased (barrel chest) due to the increased lung volume. | emphysema |
| Why do patients with emphysema have a barrel chest? | increased lung volume |
| Emphysema, Expiration is prolonged due to the lack of elastic recoil, and patients tend to exhale through pursed lips since this helps generate a | greater compressive force by the chest wall. |
| Do clients with emphysema have a mismatch of V/P? | no |
| Why do clients with emphysema not have a v/p mismatch? | lung tissue and vessels are equally destroyed. |
| When do clients with emphysema develop cyanosis? | Late stages |
| On chest X-ray, there is increased radiolucency of the lung fields with depression and flattening of the diaphragm, with what type of obstructive lung disease? | emphysema |
| This disorder is characterized by an increased sensitivity of the tracheobronchial tree to various stimuli | BRONCHIAL ASTHMA |
| Disease manifested by acute, widespread, Disease manifested by narrowing of the small airways and a more chronic narrowing of the airways due to inflammation, edema, and increased mucus production (which is more slowly responsive to treatment). | BRONCHIAL ASTHMA |
| Bronchia asthma is manifested by acute, widespread, narrowing of the small airways due to | bronchoconstriction |
| With bronchial asthma a more chronic narrowing of the airways due to | inflammation, edema, and increased mucus production |
| Which type of narrowing of airways, with bronchial asthma responds best to bronchial dilators | narrowing of small airways due to bronchioconstriction |
| This form of bronchial asthma is an IgE mediated hypersensitivity reaction (Type I) and can be triggered by a wide variety of environmental allergens. | Atopic (allergic) |
| Onset of Atopic (allergic) bronchial asthma typically occurs in | childhood |
| Is there a familial heritage of atopic/allergic bronchial constrictive asthma? | yes |
| What Serum immunoglobulin is elevated with atopic/allergic bronchial constrictive asthma? | IgE |
| immediate response of wheezing, edema, and increased mucus secretion with atopic allergic bronchial constrictive asthma is due to | degranulation of sensitized mast cells and stimulation of submucosal nerves which cause bronchoconstriction. |
| the interstitial edema resulting from allergic bronchial constrictive asthma reduces overall lung | compliance. |
| With allergic bronchial constrictive asthma, there is also a delayed response of persistent bronchospasm resulting from the recruitment of ____________which release additional chemical mediators | inflammatory cells |
| form bronchial asthma frequently triggered by upper respiratory infections (primarily viral). | Non-atopic |
| What is mechanism of action for nonatopic bronchial asthma? | unknown |
| Are IgE levels elevated with non atopic bronchial asthma? | no |
| Is there familial tendency with non atopic bronchial asthma | no |
| What is a common drug that can indue asthma | asaprin |
| Complications of what disease include status asthmaticus, respiratory failure, pneumothorax or pneumomediastinum, pneumonia, atelectasis, and mucoid impaction. | bronchial asthma |
| This is a permanent dilatation of bronchi and bronchioles resulting from inflammatory damage to their walls. | BRONCHIECTASIS |
| Causes of bronchiectasis include | bronchial obstruction, necrotizing pneumonia, congenital or inherited conditions |
| What inherited conditions is noted for causeing bronchiectasis? | cystic fibrosis |
| The inflammatory reaction in the bronchial wall, with bronchiectasis ultimately results in what three things? | weakening, abnormal dilatation, and fibrosis. |
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