Respiratory Disorders



Respiratory Disorders





ACUTE RESPIRATORY DISTRESS SYNDROME

Acute respiratory distress syndrome (ARDS) is characterized by pulmonary edema and refractory hypoxemia. ARDS can lead to multiple organ failure and has a high rate of mortality. Increased capillary permeability is the hallmark of ARDS. Diagnosis is often difficult, and death can occur within 48 hours of onset if ARDS is not promptly diagnosed and appropriately treated.


Causes

The most common cause of ARDS is sepsis. Infection, including severe sepsis and pneumonia, is the leading predisposing factor for ARDS.



  • Injury to the lung from trauma


  • Sepsis


  • Trauma-related factors, such as fat emboli, sepsis, shock, pulmonary contusions, and multiple transfusions


  • Aspiration of gastric contents, viral pneumonia


  • Anaphylaxis


  • Drug overdose


  • Idiosyncratic drug reaction to ampicillin or hydrochlorothiazide


  • Inhalation of noxious gases (nitrous oxide, ammonia, chlorine)


  • Near drowning


  • Oxygen toxicity


  • Coronary artery bypass grafting


  • Hemodialysis


  • Leukemia


  • Acute miliary tuberculosis


  • Pancreatitis


  • Thrombotic thrombocytopenic purpura


  • Uremia


  • Venous air embolism







ASTHMA

Asthma is a complex disorder of the airways that is characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation. Airflow limitation is caused by changes in the airway, causing bronchoconstriction, airway edema, and mucus hypersecretion. The National Heart Lung and Blood Institute, National Asthma Education and Prevention Program. Expert Panel Report 3 (EPR-3) recommends monitoring of clinically relevant aspects of care and the importance of planned primary care and providing patients practical tools for self-management.


Causes

The development of asthma involves interaction between genetics and environmental exposures (EPR-3, 2007; GINA, 2017). Patients who are at high risk for asthma-related death require special attention.



  • Viral infections (one of the most important causes of asthma)


  • Pollen, air pollution


  • Animal dander


  • House dust or mold


  • Kapok or feather pillows


  • Food additives, including sulfites and some dyes


  • Noxious fumes, tobacco smoke

Patients with intrinsic, or nonatopic, asthma react to internal, nonallergenic factors.



  • Irritants


  • Emotional stress and anxiety


  • Respiratory infections


  • Endocrine changes


  • Temperature or humidity variations


  • Coughing or laughing


  • Genetic factors





Asthma Control

The National Asthma Education and Prevention Program Expert Panel Report 3, (EPR-3) define asthma control as “the degree to which the manifestations of asthma symptoms, functional impairments, and risks of untoward events are minimized and the goals of therapy are met.” Every patient with asthma should be able to recognize symptoms that suggest inadequate asthma control. Written action plans detailing medications and environmental control strategies tailored for each patient are recommended for all patients with asthma.

Monitoring asthma control is the goal for asthma therapy and distinguishing between classifying asthma severity and monitoring asthma control.

Distinguishing between classifying asthma severity and monitoring asthma control.

Severity: the intrinsic intensity of the disease process. Assess asthma severity to initiate therapy.

Control: the degree to which the manifestations of asthma are minimized by therapeutic interventions and the goals of therapy are met. Assess and monitor asthma control to adjust therapy.

Impairment and Risk of Asthma:

The two key domains of severity and control are impairment and risk. The domains represent different manifestations of asthma, they may not correlate with each other, and they may respond differentially to treatment.

Impairment: frequency and intensity of symptoms and functional limitations the patient is experiencing currently or has recently experienced.

Risk: the likelihood of either asthma exacerbations, progressive decline in lung function (or, for children, lung growth), or risk of adverse effects from medication.




ACUTE BRONCHITIS

Acute bronchitis is a common, self-limiting, respiratory tract infection characterized primarily by a cough generally lasting 1 to 3 weeks. The distinguishing characteristic of bronchitis is obstruction of airflow and an inflammatory response within the epithelium of the bronchi causing airway hyperresponsiveness and increased mucus production. The inflammation occurs as a result of an airway infection or environmental triggers. The causative pathogen for bronchitis is rarely identified, although viral infections accounting for an estimated 89% to 95% cases (Tackett & Atkins, 2012). The most common viral pathogens include adenovirus, coronavirus, influenza A and B, metapneumovirus, parainfluenza virus, respiratory syncytial virus, and rhinovirus (Albert, 2010). Bacteria may cause bronchitis in people with underlying respiratory disease. Mycoplasma pneumoniae and Chlamydia pneumoniae are bacterial pathogens that primarily affect young adults. Bordetella pertussis can also lead to acute bronchitis especially in unvaccinated patients (Albert, 2010). Testing for pertussis may be warranted. Chest radiographs are indicated when acute bronchitis cannot be clinically distinguished from pneumonia. Inflammation in acute bronchitis is usually transient and resolves after the infection has subsided.

The management of acute bronchitis is primarily supportive and is focused on controlling cough. Antibiotic therapy has a minor role in acute bronchitis (Hart, 2014). Inappropriate use of antibiotics for viral respiratory infections contribute to antibiotic resistance and possible adverse events. Inhaled beta agonists should be reserved for patients with underlying pulmonary disease. Over-the-counter medications, such as dextromethorphan or guaifenesin, administered as directed in the appropriate age group may be efficacious, despite lack of substantial evidence. Antitussive therapy may be helpful for sleep distribution contributed to nocturnal cough.

Expectorants have been shown to be ineffective in the treatment of acute bronchitis (Albert, 2010). Patient education must address etiology and symptomatology, rationale for duration of cough, and appropriate medical interventions.



CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) is a common yet preventable disease characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities (GOLD, 2017). This disorder leads to airway obstruction, hyperinflation, and abnormal gas exchange causing dyspnea and functional limitation. Overlap is present between COPD and the other disorders that cause airflow limitation, such as asthma emphysema, chronic bronchitis, bronchiectasis, and bronchiolitis. Spirometry is required to make the diagnosis of COPD. The primary risk factor for COPD is cigarette smoking.

COPD should be considered in any patient who has dyspnea, chronic cough or sputum, and/or a history of exposure to risk factors for the disease (GOLD, 2017). Management for stable COPD is based on the individualized assessment of symptoms and future risk of exacerbations (GOLD, 2017).



Causes



  • Cigarette smoking


  • Exposure to irritants


  • Genetic predisposition


  • Exposure to organic or inorganic dusts


  • Exposure to noxious gases


  • Respiratory tract infection




CHRONIC BRONCHITIS

Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years with other causes of cough being excluded (GOLD, 2017). Chronic bronchitis is caused by the overproduction and hypersecretion of mucus by goblet cells. Mechanisms responsible for excessive mucus in COPD are overproduction and hypersecretion by goblet cells and decreased elimination of mucus. Chronic bronchitis leads to decreased airflow obstruction by luminal obstruction of small airways, epithelial remodeling, and decreased airway surface tension.

Chronic bronchitis causes hypertrophy of airway smooth muscle and hyperplasia of the mucous glands, increased numbers of goblet cells, ciliary damage, squamous metaplasia of the columnar epithelium, and chronic leukocytic and lymphocytic infiltration of bronchial walls. Hypersecretion of the goblet cells blocks the free movement of the cilia, which normally sweep dust, irritants, and mucus away from the airways. Accumulating mucus and debris impair the defenses and increase the likelihood of respiratory tract infections.




Diagnostic Test Results: Chronic Bronchitis



  • Chest X-rays show hyperinflation and increased bronchovascular markings.


  • Pulmonary function studies indicate increased residual volume, decreased vital capacity and forced expiratory flow, and normal static compliance and diffusing capacity.


  • ABG analysis reveals decreased partial pressure of arterial oxygen and normal or increased partial pressure of arterial carbon dioxide. ABGs provide the best evidence as to acuteness and severity of disease exacerbation.


  • Sputum analysis reveals many microorganisms and neutrophils.


  • Electrocardiography shows atrial arrhythmias; peaked P waves in leads II, III, and aVF and, occasionally, right ventricular hypertrophy.




EMPHYSEMA

Emphysema is pathologically defined as an abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls (GOLD, 2017). Airflow limitation in emphysema is due to loss of elastic recoil and decrease in airway tethering. A permanent enlargement of air spaces distal to the terminal bronchioles, emphysema leads to a significant decline in the alveolar surface area available for gas exchange. Loss of individual alveoli with septal wall destruction leads to airflow limitation. The various subtypes of emphysema include proximal acinar, panacinar, or distal acinar.

Physical examination thoracic examination reveals diminished breath sounds, diffuse or focal wheezing, diffusely, hyperresonance upon percussion, prolonged expiration, and classically a 2:1 increase in anterior to posterior diameter.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD, 2017) guidelines recommend various instruments to assess severity of symptoms, risk of exacerbations, and the presence of comorbidities, which are important to the patient’s experience of the disease and prognosis. The most widely used research tool, the St. George’s Respiratory Questionnaire (SGRQ), is a 76-item questionnaire that includes three component scores (i.e., symptoms, activity, and impact on daily life) and a total score. The GOLD guidelines suggest using the COPD Assessment Tool (CAT) or the modified Medical Research Council (mMRC) dyspnea scale.








CYSTIC FIBROSIS

Cystic fibrosis is a hereditary disorder affecting the exocrine gland and causing severe damage to multiple organ systems. Chronic progressive lung disease is the most prominent cause of morbidity and death in patients with cystic fibrosis.

Cystic fibrosis is accompanied by many complications and has a median survival rate of 31 years. The disease affects males and females and is the most common fatal genetic disease in children of European ancestry. There are more than 30,000 patients with cystic fibrosis in the United States (Cystic Fibrosis Foundation, 2017).


Cause

Inherited as an autosomal recessive trait, the responsible gene, on chromosome 7q, encodes a membrane-associated protein called the cystic fibrosis transmembrane regulator (CFTR). The exact function of CFTR remains unknown, but it appears to help regulate chloride and sodium transport across epithelial membranes.

Sep 22, 2018 | Posted by in ANATOMY | Comments Off on Respiratory Disorders
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