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Paper 3
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Acute respiratory distress syndrome (ARDS) is caused by diffuse alveolar damage leading to bilateral pulmonary oedema with normal hydrostatic pressures, that is non-cardiogenic oedema. Typically this causes patchy, peripheral consolidation rather than the perihilar oedema seen in cardiac and renal failure. Cardiomegaly and prominent pulmonary vessels would not be expected, and pleural effusions and interstitial lines are also less frequent than in cardiac or renal failure, although some patients may have a mix of underlying pathologies. Often on CTs of ITU patients with ARDS, the ground glass consolidation is more marked in the dependent region of the lungs, which protects this region from barotrauma caused by ventilation. Hence the long-term fibrotic changes associated with the condition are typically anteriorly distributed, although many patients do not demonstrate any significant chronic pulmonary changes.
Effects of treatment on the thorax
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Dhakshina Moorthy Ganeshan, Herman I Libshitz, Revathy B Iyer
Bleomycin, busulphan, and methotrexate are recognized to cause pulmonary parenchymal injury independent of associated radiotherapy (18). The toxicity is related to accumulation of drugs in the lung and is directly related to the cumulative dose administered (18). The use of concomitant radiation, other chemotherapy, or oxygen therapy compounds the pulmonary toxicity. Early changes on chest radiography include a reticulonodular interstitial pattern, which is initially seen in the basal segments. Lung injury may be progressive, resulting in alveolar damage and eventual pulmonary fibrosis (19). Busulphan may cause interstitial lung damage, resulting in a reticular pattern on conventional radiographs (19). Methotrexate is used in the treatment of leukaemia and other malignancies. A hypersensitivity reaction may occur, resulting in alveolar infiltrates. The diffuse alveolar damage may result in fibrosis (19). Mediastinal adenopathy may also occur.
Embolism, Ischaemia, Infarction and Shock
Published in Jeremy R. Jass, Understanding Pathology, 2020
In a state of shock the organs at greatest risk are the brain, heart, lungs, kidneys, gut and adrenals. If the patient survives, ischaemic loss of neurons and myocardial cells is irreversible. The kidney is susceptible to the development of acute tubular necrosis which presents with renal failure, however, regeneration of renal tubules may occur with complete recovery of renal function. Shock caused by bacterial sepsis or severe trauma may result in diffuse alveolar damage of the lungs, a condition known as shock lung or adult respiratory distress syndrome (ARDS). The alveolus becomes lined with a hyaline (amorphous pink) membrane composed of fibrin which interferes with gaseous exchange. If the patient survives, the fibrin may either be removed or organised into fibrous tissue, which may lead to the development of ‘honeycomb lung’ (page 214). The adrenals show a characteristic shock sequence in which the yellow lipid of the cortical cells is converted into steroid hormones and therefore disappears.
COVID-19: captures iron and generates reactive oxygen species to damage the human immune system
Published in Autoimmunity, 2021
SARS-CoV-2 infection can activate abnormal inflammation and immune response [4], which is manifested by increased levels of IL-6, IL-1β, IL-8, IL-17, G-CSF, GM-CSF, IP10, MCP1, MIP1α, TNF, C-reactive protein and D-dimer. Extremely high levels of pro-inflammatory cytokines can give rise to the cytokine storm, causing local or systemic tissue damage—excessive dimer and cellulose levels for extensive capillary coagulation reactions [31]. Inflammation and blood clotting occur in multiple types of organs, such as lungs, heart, kidneys, nervous system, bone marrow and vessels. According to relevant autopsy report, the novel coronavirus pneumonia is an extremely destructive disease and SARS-CoV-2 particles are detected in the patient’s respiratory system, kidneys and gastrointestinal tract [32]. Moreover, lungs are infiltrated by massive macrophages and monocytes, and the amount of polykaryocyte cells is still large. There are likewise a few lymphocytes, eosinophils and neutrophils. The lymphocytes are dominated by positive CD4 +T cells [33]. Moreover, the lesions are all manifested as diffuse alveolar damage, accompanied by fibrin membrane formation and fibrin clumps in the alveoli [34]. In addition, hyaline membrane formation, fibrin exudate, epithelial damage and diffuse-type II lung cell hyperplasia are also found in the lungs [35]. Inflammation and fibrin microthrombus appear in the tissues around the heart capillaries, liver sinuses and renal tubules [36]. Taken together, these features show that viruses also damage the human immune system, directly or indirectly causing these severe diseases.
Histologic patterns of lung injury in patients using e-cigarettes
Published in Baylor University Medical Center Proceedings, 2020
Samreen Fathima, Haiying Zhang
Only a few articles have described the pathology in vaping-associated injury. From a histologic standpoint, the patterns commonly seen are diffuse alveolar damage and organizing pneumonia.1 A spectrum of acute lung injury can be observed, including mucopolysaccharide-rich intraluminal plugs of proliferating fibroblasts within alveolar spaces and distal bronchioles (organizing pneumonia); diffuse alveolar septal thickening, type II pneumocyte hyperplasia, and hyaline membranes (diffuse alveolar damage); and abundant intra-alveolar fibrin accompanied by alveolar septal edema and variable degrees of organization with acute fibrinous and organizing pneumonia. Other patterns associated with vaping include acute alveolar hemorrhage, acute eosinophilic pneumonia, and hypersensitivity pneumonia. Some nonspecific findings such as foamy macrophages and foamy pneumocytes are also seen, which could also be due to other causes such as toxic fume injury or use of amiodarone. Some neutrophils and eosinophils were reported in recent case series.1,6,10
The acute respiratory distress syndrome
Published in Baylor University Medical Center Proceedings, 2020
Christopher Wood, Vivek Kataria, Ariel M. Modrykamien
In a normal healthy lung, fluid movement is regulated to keep the alveoli dry and hold on to a small amount of interstitial fluid. Lung injury, such as ARDS, disrupts this regulatory process, resulting in diffuse alveolar damage.17 One form of ventilator-induced injury, referred to as “biotrauma,” can happen in both healthy and injured lungs.18 It causes a systemic inflammatory response releasing a cascade of cytokines.18 Three general regions of the lung have been described in ARDS: normal lung tissue, densely consolidated lung, and a collapsible region during expiration that is recruitable during inspiration.19 In the absence of optimal PEEP, this collapsible/recruitable region of the lung can form an injury known as “atelectrauma” due to the repeated opening and closing of the airway and alveoli.20 Proposed methods to determine optimal PEEP will be discussed further.