Disease Flashcards
What is pulmonary edema?
Pulmonary edema is a potentially lifethreatening edema in the interstitium and alveoli of the lungs. The collected fluid may block the exchange of oxygen and carbon dioxide and produce respiratory failure.
Causes: Fluid may seep out of the alveolar capillaries if these blood vessels are damaged and become excessively permeable to liquids (noncardiogenic pulmonary edema) or if hydrostatic pressures within blood vessels exceed the strength of the normal alveolar capillary wall (cardiogenic pulmonary edema). Cardiogenic pulmonary edema can result from any condition that compromises left ventricular function, causing elevations in pulmonary venous, and capillary hydrostatic pressures (congestive heart failure), including myocardial infarction, ischemia, or myocardial stunning; severe valvular heart disease; arrhythmias; excessive intravenous fluid administration; and diastolic dysfunction. Noncardiogenic pulmonary edema usually results from blood vessel injury, as happens in the adult respiratory distress syndrome (sepsis, shock, aspiration pneumonia, airway obstruction). Occasionally, protein-rich fluid floods the lungs from drug exposure (such as heroin overdose), hypoalbuminemia, high-altitude exposure (mountain sickness), fresh water aspiration in near drowning, hemorrhage in or around the brain, or other conditions. Pulmonary edema can occur as a chronic or acute condition.
Symptoms: Chronic symptoms of heart failure include dyspnea on exertion, nocturnal dyspnea, orthopnea, and cough. When pulmonary edema develops rapidly, patients experience a rapid onset of shortness of breath and suffocation and often demonstrate labored, noisy breathing; cough producing frothy, bloody sputum; gasping; anxiety; palpitations; and altered mental status caused by inadequate oxygenation. Signs of the condition include a rapid respiratory rate, heaving of the chest and abdomen, intercostal muscle retractions, diffuse crackles on lung examination, and, often, cold, clammy skin with diaphoresis and cyanosis. Tachycardia, jugular vein distention, and a diastolic (S3) gallop occur. As cardiac output decreases, the pulse becomes thready, and blood pressure falls. Pulmonary artery catheterization helps identify left-sided failure (elevated pulmonary wedge pressures), and arterial blood gases show hypoxia. Profound respiratory alkalosis occurs when patients hyperventilate when trying to increase their oxygenation; acidosis may occur with respiratory fatigue or failure. To improvement the movement of air into and out of the chest, the patient will often sit upright to breathe and resist lying down.
Diagnosis: Patients who are short of breath and who have pulmonary rales, low oxygen saturation rates, and/or a history of heart disease should have a chest x-ray taken urgently, to see if they may have characteristic findings of pulmonary edema on radiography. These findings include an enlarged heart shadow, central congestion, and pulmonary effusions. The diagnosis of acute pulmonary edema can be aided by evidence of an elevated beta natriuretic peptide (BNP), or the results of echocardiography, although these tests are usually not required to establish the diagnosis. In patients who do not have a history of heart disease or acute cardiac decompensation, noncardiogenic pulmonary edema may present as dyspnea, rales, and impaired oxygenation without cardiomegaly or a reduction in cardiac ejection fraction
Venes, Donald. Taber’s Cyclopedic Medical Dictionary (p. 775). F.A. Davis Company. Kindle Edition.
What is acute respiratory distress syndrome (ARDS)?
Acute respiratory distress syndrome (ARDS) is respiratory insufficiency marked by progressive hypoxemia due to severe inflammatory damage causing abnormal permeability of the alveolocapillary membrane. The alveoli fill with fluid, which interferes with gas exchange.
Etiology: ARDS may result from direct trauma to the lungs, e.g., near drowning, aspiration of gastric acids, severe lung infection or systemic disorders, e.g., shock, septicemia, disseminated intravascular coagulation (DIC), cardiopulmonary bypass, or reaction to blood transfusions. Widespread damage to the alveolocapillary membranes is initiated through the aggregation and activity of neutrophils and macrophages and the activation of complement. Cytokines, oxygen-free radicals, and other inflammatory mediators damage the walls of capillaries and alveoli, producing diffuse inflammatory interstitial and alveolar edema, fibrin exudates, and hyaline membranes that block oxygen delivery to the blood.
Diagnosis: Diagnosis is based on a history of a recent event associated with the onset of ARDS, the presence of noncardiogenic pulmonary edema on the chest radiograph, and persistent hypoxemia and a PaO2/FIO2 ratio of 200.
Symptoms: Dyspnea and tachypnea are followed by a progressive hypoxemia that, despite oxygen therapy, is the hallmark of ARDS. Diffuse, fluffy infiltrates can be seen on chest radiographs as inflammation increases alveolar permeability, causing visible alveolar flooding and collapse.
Treatment: Endotracheal intubation, mechanical ventilation with positive end-expiratory pressure (PEEP), supplemental oxygen, and tidal volumes of 4 to 8 ml/kg optimize respiratory outcomes. PEEP increases intrathoracic pressure, keeping alveoli open during exhalation. This reduces the pressure required to open alveoli during inhalation, improves gas exchange, and reduces oxygen need. The patient should be monitored and treated for acidosis, cardiac arrhythmias, DIC, oxygen toxicity, renal failure, and sepsis. Placing the patient in the prone position reduces mortality.
What is pneumonitis?
Pneumonitis is inflammation of the lung, usually due to hypersensitivity (allergy), radiation exposure, aspiration, viral infection, or autoimmune illnesses, such as systemic lupus erythematosus.
What is hypersensitivity pneumonitis?
Hypersensitivity pneumonitis is immunologically induced pneumonitis in a susceptible host caused by repeated inhalation of a variety of substances including organic dusts. Included are molds and other fungi from sources such as cheese, vegetables, mushrooms, flour, mushroom compost, bark of trees, detergents, and contaminated humidification systems. In the acute stage, patients may present with cough, fever, chills, malaise, and shortness of breath. In the subacute and chronic forms, the onset of symptoms is gradual and prolonged. Treatment includes identifying and avoiding causative agents.
*Lung biopsy in hypersensitivity pneumonitis reveals o infiltrate with poorly formed noncaseating granuloma, and interstitial fibrosis (chronic pneumonitis only).
What is idiopathic pulmonary fibrosis (IPF)?
Idiopathic pulmonary fibrosis (IPF) the formation of scar tissue in the parenchyma of the lungs, following inflammation of the alveoli. The disease results in difficulty breathing caused by impaired gas exchange.
Symptoms: Dyspnea, cough, exertional fatigue, and generalized weakness are common. Signs of the illness include pulmonary crackles, finger clubbing, cyanosis, and evidence of right ventricular failure (such as lowerextremity swelling). The disease typically progresses to end-stage lung disease and death within 7 years of diagnosis.
Diagnosis: A biopsy of the lung is needed to make the diagnosis.
Treatment: Corticosteroids (such as prednisone) may be helpful in 10% to 20% of patients. Lung transplantation can be curative if a donor organ is available.
Microscopic findings of IPF are heterogeneous and include:
-Patchy areas of interstitial fibrosis with chronic interstitial inflammation intermixed with normal lung
-Early lesions consist of fibroblastic foci that become increasingly collagenous with time
-Honeycomb pattern with fibrotic walls and cystic spaces lined by bronchiolar epithelium
-Fibrosis most prominent in the subpleural and perilobular regions
