Week 5 Flashcards
Discuss the role of alveolar epithelial cells and fibroblasts in the proposed pathogenic mechanism of usual interstitial pneumonia
In the proposed pathogenic mechanism of this disease, alveolar epithelial cells are injured by environmental factors, which interact with genetic or aging-related factors to produce persistent epithelial injury. Factors secreted from injured alveolar epithelial cells activate interstitial fibroblasts to proliferate and produce collagen. The dense fibrosis causes destruction of alveolar architecture and formation of cystic spaces
Describe three risk factors that may interact to cause the initial injury in the proposed pathogenic mechanism of usual interstitial pneumonia
In the proposed pathogenic mechanism of this disease, alveolar epithelial cells are injured by environmental factors, which interact with genetic or aging-related factors to produce persistent epithelial injury.
Environmental factors include cigarette smoking, occupational exposures (ex. farming, hair-dressing, stone-polishing), environmental toxins and viral infections.
Genetic factors include inherited genetic mutations involving telomerase, surfactant and MUC5B mucin.
Age-related factors may be associated with telomere shortening or from some other unknown acquired change associated with aging.
Discuss how the patient’s mean pulmonary arterial pressure would be altered during exercise.
Typically with exercise, the mean pulmonary arterial pressure will decrease as a response to recruitment and distention of more pulmonary vessels. However, this patient’s pulmonary fibrosis is associated with a narrowing of her pulmonary vessels and increased pulmonary vasculature resistance. These pathological changes to the vessels structure impedes the ability of recruitment and distention of the pulmonary vasculature. As a result, her mean pulmonary arterial pressure would stay elevated during exercise.
Explain the effect that this patient’s pulmonary fibrosis has on the diffusion capacity of carbon monoxide (DLCO).
This patient has pulmonary fibrosis which increases the thickness of the alveolar-capillary barrier. The diffusion capacity of carbon monoxide (DLCO) measures the rate by which carbon monoxide is absorbed from the alveoli into the pulmonary capillaries. Because the diffusion properties of the alveoli-capillary barrier is increased, the rate of diffusion would decrease resulting in the reduced DLCO.
Compare and contrast the typical management of Usual Interstitial Pneumonia (UIP) and Nonspecific Interstitial Pneumonia (NSIP).
In any case of Idiopathic Interstitial Pneumonia (IIP), [which includes both UIP (idiopathic pulmonary fibrosis-IPF) and NSIP] any causative exposure(s) should be identified and eliminated. Supportive care for UIP and NSIP typically consists of pulmonary rehabilitation and consideration of oxygen supplementation. Palliative care and/or lung transplantation may be considered for more severe/advanced cases.
In diseases such as UIP (IPF), what was once thought to be standard of care (prednisone plus azathioprine) has been demonstrated to carry harm without potential for benefit. In contrast to UIP, NSIP (as well as Cryptogenic Organizing Pneumonia and connective tissue disease–associated ILD) may respond favorably to corticosteroids and other immunosuppressive agents.
J68-year-old female develops marked dyspnea, tachypnea, and acute respiratory failure 24-hours after being admitted to the hospital for pneumonia. Chest X-ray shows diffuse bilateral alveolar infiltrates, and her PaO₂/FiO₂ ratio is 109 (>200). Justify the patient’s predicted ventilation and perfusion (V/Q) ratios.
In this patient, there would be areas of shunting and low V/Q matching as a result of ARDS. This is because destruction of the type II alveolar epithelial cells decreases the formation of pulmonary surfactant. This increases surface tension on the alveoli causing atelectasis. The result is absolute intrapulmonary shunts (V/Q = 0), in which, mixed venous blood is perfusing totally unventilated or collapsed alveoli.
Damage to the type I alveolar epithelial cells and pulmonary capillary endothelial cells leads to the formation of the interstitial and intra-alveolar edema. This in combination with the debris from the dead alveolar cells induces the organization of hyaline membranes causing nonuniform ventilation resulting in areas with shunt-like states (low V/Q ratios).
Correlate this patient’s reduced functional residual capacity (FRC) to the pathogenesis of acute respiratory distress syndrome (ARDS).
ARDS is associated with pneumocyte and pulmonary endothelium injury. The pneumocyte injury is sensed by the resident macrophages stimulating the release of proinflammatory cytokines. These activate the pulmonary endothelial cells causing increased expression of adhesion molecules. Neutrophils adhere to the activated endothelial cells and migrate into the interstitium and alveoli. Upon degranulation, the neutrophils release inflammatory mediators, including reactive oxidative species, leading to further endothelial injury.
This vicious cycle of inflammation and endothelial damage increases pulmonary capillary permeability. This causes formation of interstitial and intra-alveolar edema. Damage and necrosis of the type II alveolar cells leads to pulmonary surfactant abnormalities. The combination of these exaggerate the surface tension forces reducing the compliance of the lung. The increase in elastic recoil of the lung is greater than the outward elastic recoil of the chest wall. This causes the lung-chest wall unit to move to a lower volume at the end of expiration reducing the FRC.
The patient develops a left-sided pleural effusion. Identify the recommended anatomical location to safely place a thoracentesis needle to drain the fluid. Explain your rationale.
To avoid damage to the intercostal nerve and vessels, the needle is inserted superior to the rib, high enough to avoid the intercostal nerve, artery, and vein. When the patient is in the upright position, intrapleural fluid accumulates in the costodiaphragmatic recess. Inserting the needle into the 9th intercostal space in the midaxillary line during expiration will avoid the inferior border of the lung.
Correlate this patient’s diagnosis with her presenting symptoms (to include the physiologic basis for the noted symptoms), the biopsy findings, her management options, and her prognosis.
This patient’s presentation and biopsy result are typical for carcinoid tumor. Since there is no necrosis, cytologic atypia or increased mitotic activity, atypical carcinoid tumor or a more concerning lesion is not likely.
Cough and hemoptysis may be associated with any lung tumor involving an airway, and these findings are related to the mechanical irritation caused by the tumor involving and partially obstructing the bronchus. The finding of post-obstructive pneumonia is also compatible with the physical effects of tumor. The associated symptoms of flushing, cyanosis and diarrhea are typical of the carcinoid syndrome. This is a paraneoplastic syndrome caused by secretion of vasoactive amines by carcinoid tumors, most prominently serotonin and kallikrein.
In most cases, early stage carcinoids may be treated surgically, with a good prognosis.
On examination her physician finds bilateral rib 8-12 exhalation dysfunctions. Describe the normal biomechanical movements of the involved rib regions.
The vertebral and sternal attachments of ribs 1-7 and the vertebral and chondral attachments of ribs 8-10 combine to promote specific vectors of motion during normal inhalation, expanding the chest. This expansion moves through two major vector paths. These patterns are described as occurring through pump-handle and bucket-handle axes in both vertebrosternal ribs 1 to 7 and vertebrochondral ribs 8 to 10.
In the described dysfunctional area, the primary motion of ribs 8-10 would be “bucket handle.” During inhalation, ribs rotate on their anterior and posterior attachments allowing the rib to move lateral and superior in inhalation and medial and inferior in exhalation.
The eleventh and twelfth ribs have only costovertebral articulations. Because there are no transverse process limitations, the motion of these ribs is caliper-like along a horizontal plane. This motion produces slight changes in both the anteroposterior and the transverse dimensions. The ribs move inferior and “open” laterally in inhalation and superior and “close” medially in exhalation.
health risks of inhaled tars. Identify the source, the production, and the primary harmful effect of inhaled hydrocarbons.
Cigarette smoke contains a vast number of harmful chemicals, including polycyclic aromatic hydrocarbons (PAHs) such as benzopyrenes (as well as over 500 other PAHs such as naphthalene, fluorene, phenanthrene, fluoranthenes, and anthracenes).
Such hydrocarbons are produced from incompletely combusted organic matter – in this case, tobacco.
PAHs are carcinogens, and local administration/inhalation is well-known to induce lung cancer (as a representative example, Benzo[a]pyrene (BaP) is a Group 1 carcinogen, which classifies it as the most potent carcinogen among the PAHs).
Justify how the patient’s cigarette smoking would alter the P50 of the oxyhemoglobin curve.
One of the major components of cigarette smoke is carbon monoxide (CO) which interferes with the oxygen transport function of blood by combining with hemoglobin to form carboxyhemoglobin. Therefore, smokers have increased levels of carboxyhemoglobin. Because it has more than 200 times the affinity to hemoglobin in comparison with oxygen, it will combine with the same amount of hemoglobin as oxygen when the PCO is 200 times lower. Therefore, small amounts of CO can tie up large portions of hemoglobin in the blood, making it less available for oxygen carriage. In this state, those oxygen molecules that do bind to hemoglobin, bind with greater affinity. This would result in a decreased P50 (i.e. left shift) of the oxyhemoglobin curve.
The patient’s primary care physician initiates motivational interviewing to discuss smoking cessation, and during the course of the conversation, the patient voices change talk consisting of statements like “I know I have to quit so I don’t end up with lung cancer,” and “I’ve been doing OK cutting back lately.” List the categories of change talk expressed by this patient.
The first half of the patient’s first statement (“I know I have to quit…”) is considered a Need.
The second half of the patient’s first statement (“…so I don’t end up with lung cancer”) is considered a Reason.
The first half of the patient’s second statement (“I’ve been doing OK…”) is considered an Ability.
The second half of the patient’s second statement (“…cutting back lately”) is considered (Already) Taking Steps.
Justify the patient with PE that has a normal PCO2 but decreased PO2.
Although there is significant alveolar dead space due to the pulmonary emboli, her arterial PCO2 remains normal because of her increased ventilation rate. Peripheral chemoreceptors sense the changes in arterial PCO2 and stimulate the respiratory control system to increase minute ventilation. This ventilatory response is potentiated by hypoxia.
Describe the role of the pulmonary arteries within the pulmonary circulation and explain the signs and symptoms in this patient that would correlate to her pulmonary embolism.
The pulmonary arteries are part of the pulmonary circulation that extend from the heart to the lungs. The left pulmonary artery (LPA) directs blood to the left lung, while the right pulmonary artery directs blood to the right lung. The LPA connects to the left lung and branches into smaller vessels such as the interlobular arteries within the lung. The role of the pulmonary arteries is to deliver deoxygenated blood to the lungs to acquire oxygen.
Pulmonary embolism occurs when a blood clot in a leg vein (venous thromboembolism) breaks loose and travels to a lung (pulmonary) artery and blocks blood flow. Reduced blood flow to one or both lungs can cause the patient’s shortness of breath. Inflammation of the tissue covering the lungs and chest wall (pleura) could have caused sharp chest pain. The patient’s leg edema is a result of the venous occlusion. The increase in the patient’s heart rate and respiratory rate are compensatory responses to the reduced cardiac output and impaired gas exchange induced from the pulmonary embolism.
