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Cardiac Hypertrophy, Heart Failure and Cardiomyopathy
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Myocardial fibrosis occurring both as macroscopic or microscopic scarring in subjects who do not have chronic cardiac failure or RCM clinically, but who suffer sudden death present a pathological challenge and is usually labelled as idiopathic fibrosis if there is no previous clinical history. Fibrosis is the end-stage of a wide variety of mechanisms of cardiac damage and thus a specific diagnosis may not be possible. Some of these will be revealed by the previous medical history, i.e. radiation or scleroderma, in others, their pathogenesis remains unknown. Ischaemic scarring is usually recognized by the presence of severe coronary artery stenosis and a regional pattern.
Inhalation Toxicity of Metal Particles and Vapors
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Prolonged inhalation of fine dust may considerably decrease the total absorptive capacity of the lungs. When industrial dusts accumulate in the bronchioles, the irritation reaction may include formation of fibrosis with subsequent dysfunction of that portion of the lung. This fibrosis may result in increased toxicity. Partial blockage tends to decrease pulmonary circulation, making the bronchial circulation important in absorption. Material absorbed in the bronchial arteries and veins goes directly from the arterial blood to tissues without benefit of the slow filtration through the reticuloendothelial components of lymphatic or pulmonary capillaries. The pulmonary blood is therefore a potentially dangerous pathway for absorption of metals in persons with lung dys-function.
General Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Rebecca Fish, Aisling Hogan, Aoife Lowery, Frank McDermott, Chelliah R Selvasekar, Choon Sheong Seow, Vishal G Shelat, Paul Sutton, Yew-Wei Tan, Thomas Tsang
How is lymphoedema staged?Lymphoedema is staged using the International Society of Lymphology (ISL) lymphoedema stagingStage 0: Subclinical lymphoedema. No obvious swelling despite impaired lymph transport.Stage I: Limb swelling which resolves with limb elevation.Stage II: Limb swelling and pitting oedema not responsive to elevation. As the condition progresses patients may develop tissue fibrosis. Increased risk of soft-tissue infections.Stage III: Fibrotic tissue, oedematous limb, no pitting. Associated with skin changes including: thickening, hyperpigmentation, fat deposition, papillomas and deep skin folds.
Adverse pulmonary effects after oral exposure to copper, manganese and mercury, alone and in mixtures, in a Spraque-Dawley rat model
Published in Ultrastructural Pathology, 2023
M Draper, Mj Bester, M Van Rooy, Hm Oberholzer
In conclusion, all the heavy metal groups demonstrated toxic effects on pulmonary morphology and ultrastructure that will most likely alter physiological functioning. In all experimental groups, the metals had a negative impact on the pulmonary tissue with Cu + Hg and Mn causing the most severe and second most severe effects on pulmonary morphology, respectively. The Cu + Hg group demonstrated great yellow-red birefringence in the pulmonary tissue, indicating the development of late fibrosis. Fibrosis directly affects the physiological functioning of tissue and organs, while indirectly affecting organ systems and the functioning of the body leading to associated disease. Ultrastructurally, the pulmonary tissue had the highest sensitivity to the triple mixture group that caused the most alterations to elastin and collagen fiber bundles. Overall, Mn in any mixture caused deleterious effects with the Mn + Hg group showing the highest toxicity, which is probably mediated by increased ROS production that causes damage to membranes and the mitochondria.
An expert overview of pulmonary fibrosis in sarcoidosis
Published in Expert Review of Respiratory Medicine, 2023
Rohit Gupta, Jin Sun Kim, Robert P Baughman
A critical risk factor for development of fibrosis is non-resolving inflammation [24]. Although the pathophysiology of fibrosis is not clearly understood, studies have found associations between fibrosis development and changes in transforming growth factor-B, macrophage switching, and Th1 to Th2 transition [25,26]. As regulatory T-cells are activated, acute phase proteins like serum amyloid A are secreted, triggering a cascade of pro-inflammatory cytokines to amplify inflammation [27–29]. On histopathology, fibrotic changes seen in end-stage pulmonary sarcoidosis are distinct from that of usual interstitial pneumonia seen in idiopathic pulmonary fibrosis [30–33]. Patients with fibrotic sarcoidosis have lymphangitic distribution of fibrosis, rare foci of fibroblasts or architectural distortion, and the presence of granulomatous inflammation. Explanted lungs from patients with advanced pulmonary sarcoidosis undergoing transplantation similarly found fibrosis along a central and peribronchovascular distribution, granulomatous involvement in all compartments (parenchyma, vasculature, pleura, and lymph nodes) suggesting widespread but variable involvement of granulomatous inflammation and fibrosis in end-stage pulmonary sarcoidosis (Figure 2) [34]. Some patients can have a usual interstitial pneumonitis pattern with fibroblastic foci [30,32]. This subgroup of progressive fibrosis in sarcoidosis needs further study.
Macrophages-microenvironment crosstalk in fibrostenotic inflammatory bowel disease: from basic mechanisms to clinical applications
Published in Expert Opinion on Therapeutic Targets, 2022
Juanhan Liu, Wenbin Gong, Peizhao Liu, Yangguang Li, Haiyang Jiang, Xiuwen Wu, Yun Zhao, Jianan Ren
Fibrosis can affect any system and even lead to death[2]. Intestinal fibrosis is a common complication of IBD, including Crohn’s disease (CD) and ulcerative colitis (UC). In clinical practice, the stricture is much more common in CD, with about half of them suffering from it after 20 years of disease progression[3]. In CD, strictures are predominantly located in the terminal ileum but are far less common in the colon (around 8%). Stricture in the colon always has a high risk of colon cancer. But in UC, most colonic stricture formation is benign, with stricture incidence ranging from 1% to 11.2%[4]. Previously, fibrosis was believed to be an irreversible result of persistent inflammation. However, recent basic studies and clinical trials have revealed that fibrosis is a highly dynamic process and can be reversed[5].