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The Digestive (Gastrointestinal) System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Glands in the fundus primarily secrete hydrochloric acid and pepsin, while those in the cardia and pylorus primarily secrete mucous. Hydrochloric acid serves to release the digestive enzyme pepsin, which breaks down protein into amino acids. The mucus serves as a coating to protect the stomach lining from damage by the acid and enzymes. Hypersecretion refers to excessive amounts of these digestive enzymes.
Investigation of Pituitary Disease
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Thozhukat Sathyapalan, Stephen L. Atkin
Sellar masses are commonly encountered as incidental findings on MRI, and most of these are incidentalomas. In the absence of hormone hypersecretion, these small lesions can be safely monitored by MRI, which is performed annually and then less often if there is no evidence of growth. Resection may be considered for incidentally discovered macroadenomas, as about one-third become invasive or cause local pressure effects. If hormone hypersecretion is evident, specific therapies are indicated. When larger masses (>1 cm) are encountered, they should also be distinguished from non-adenomatous lesions including meningiomas (associated with bony hyperostosis), craniopharyngiomas (usually calcified and hypodense) and gliomas (hyperdense on T2-weighted images).
The accessory organs: Pancreas, liver and gallbladder
Published in Paul Ong, Rachel Skittrall, Gastrointestinal Nursing, 2017
Cholesterol is insoluble in water and its solubility is dependent upon the detergent properties of bile salts and phospholipids. An excess of biliary cholesterol in relation to bile salts and phospholipids can result from hypersecretion of cholesterol, or from hyposecretion of bile salts or phospholipids. The most common cause of supersaturation is cholesterol hypersecretion (Einarrson et al., 1985; Nisell et al., 1985). Hypersecretion could be caused by increased hepatic uptake of cholesterol, commonly associated with obesity, or increased hepatic synthesis of cholesterol. In non-obese individuals the development of cholesterol-rich gallstones is associated with reduced bile salt circulation within the liver.
Gut-derived bacterial flagellin induces beta-cell inflammation and dysfunction
Published in Gut Microbes, 2022
Torsten P.M. Scheithauer, Hilde Herrema, Hongbing Yu, Guido J. Bakker, Maaike Winkelmeijer, Galina Soukhatcheva, Derek Dai, Caixia Ma, Stefan R. Havik, Manon Balvers, Mark Davids, Abraham S. Meijnikman, Ömrüm Aydin, Bert-Jan H. van den Born, Marc G. Besselink, Olivier R. Busch, Maurits de Brauw, Arnold van de Laar, Clara Belzer, Martin Stahl, Willem M. de Vos, Bruce A. Vallance, Max Nieuwdorp, C. Bruce Verchere, Daniël H. van Raalte
While obesity is linked to insulin resistance, it is failure of pancreatic beta-cells that drives hyperglycemia and subsequent type 2 diabetes (T2D)1. Although in later stages of T2D insulin secretory rates are lowered, prior to the diagnosis and in earlier phases of the disease, insulin secretion is actually increased.2 Insulin hypersecretion, particularly in the fasted state, is considered harmful as it is associated with impaired proinsulin processing, insulin secretory stress and depletion of intracellular insulin stores,3 further promoting obesity and T2D development.4 Drivers of hyperinsulinemia are still elusive but could relate to islet-exposure to excessive nutrients such as carbohydrates and lipids,5 as well as a chronic low-grade inflammatory response known to be present in beta cells of people with T2D.6 In this regard, an influx of pro-inflammatory macrophages in islets of people with T2D has been noted.7 These macrophages produce pro-inflammatory cytokines such as interleukin (IL)-1β and IL-6, which have been associated with insulin hypersecretion8 and beta-cell failure.7 The triggers that ignite beta-cell inflammation in T2D remain presently unknown.
Lacrimal gland botulinum toxin injection for epiphora management
Published in Orbit, 2022
Johnathan Jeffers, Katherine Lucarelli, Sruti Akella, Pete Setabutr, Ted H. Wojno, Vinay Aakalu
Epiphora can be separated into two broad categories based on etiology: arising from either decreased tear outflow or hypersecretion from the lacrimal gland. These two etiologies are often subdivided in the literature as non-functional and functional epiphora, respectively. Functional epiphora here refers to lacrimal drainage dysfunction in the presence of anatomical patency.3 In contrast, epiphora resulting from any obstruction or other cause of decreased outflow within the lacrimal system can be characterized as non-functional epiphora. Decreased outflow may result from either lid malposition, decreased blink function, or outflow obstruction. Obstruction may result from a variety of causes including congenital ductal obstruction, prior inflammation due to infection or other inflammatory disorder, anatomic obstruction due to a tumor or other mass, and trauma. Hypersecretion results from overactivation of the lacrimal gland, especially reflex tearing. Causes include gustatory epiphora resulting from aberrant 7th nerve regeneration and reflex epiphora from ocular surface trauma or stimulation. Still, the disorder can be thought of as an interplay between these two non-mutually exclusive causes, wherein the overall aqueous tear influx and outflux of the lacrimal system must remain in balance to work effectively and any alteration to the equilibrium can result in dysfunctional epiphora.
Relevance of KISS1 gene polymorphisms in susceptibility to polycystic ovary syndrome and its associated endocrine and metabolic disturbances
Published in British Journal of Biomedical Science, 2020
MH Daghestani, MH Daghestani, M Daghistani, K Ambreen, MN Almuammar, LM Al Neghery, AS Warsy
In some studies, the most evident endocrine disturbances in PCOS were reported as LH hypersecretion, increased value of LH-FSH ratio and low or normal level of FSH [31]. Some women with PCOS also experienced high level of oestradiol with dysfunctional uterine bleeding [32]. In our present study, the PCOS group revealed the features of endocrine disturbances through increased level of LH, oestradiol and LH-FSH ratio with normal level of FSH, as compared to controls. When the influence of genotypes of rs1213704663 was investigated on the levels of the endocrine and metabolic parameters, no effect was seen on the latter. However, the GG genotype showed significantly higher level of LH, oestradiol and LHFSH ratio as compared to CG and CC genotypes, while, FSH level showed no significant difference among the genotypes of rs1213704663. These results show that the variant GG rs1213704663, influences endocrine levels in PCOS.