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Gastrointestinal Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Gareth Davies, Chris Black, Keeley Fairbrass
If organic causes have been ruled out by 1–4, possible explanations are: Gastroparesis (abnormal gastric emptying due to neuromuscular pathology, one cause being diabetic autonomic neuropathy): Barium meal and follow-through will often demonstrate abnormal gastric emptying. Some centres offer specialized gastric emptying studies.Mechanical obstruction of proximal small bowel (beyond reach of gastroscopy): Barium meal and follow-through and abdominal CT are often diagnostic.Psychological/psychiatric disease (e.g. anorexia nervosa (AN)/bulimia, severe anxiety): Diagnosis is made on typical history and exclusion of organic causes.Functional causes: This is when the cause is unknown, but the key problem is disordered upper GI motility. Cyclical vomiting syndrome gives characteristic story (see 4 above), but otherwise diagnosis is by a process of elimination.
StomachGastric Secretions, Motility, Digestion and Vomiting
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The antral activity is influenced by gastric volume, gastrin and the composition/volume of chyme entering the duodenum. Normally, liquids empty from the stomach faster than solids, with a half-time of about 20 minutes. The half-time for gastric emptying of solid food is approximately 2 hours, with less than 10% being emptied after 4 hours. Increased gastric volume produces distension, which provokes vagovagal excitatory reflexes leading to increased antral pump activity and hence gastric emptying (Figure 34.1). Both increased antral distension and high protein content of food stimulate gastrin secretion, which enhances gastric emptying.
Digestive and Metabolic Actions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
As illustrated in Figure 8.3, GI dysfunction is the most common non-motor symptom of PD [14]. Patients often have early satiety and nausea symptoms resulting from delayed gastric emptying, bloating from poor small bowel coordination, as well as constipation and defecation dysfunctions because of impaired colonic transit. Dopaminergic-related disturbances in gut motility have also been observed in transgenic mice lacking D2R [15]. These mice are smaller in size than wild-type littermates in spite of eating significantly more. They have greater defecation frequency, larger water content and mass of their stool, and significant decreases in total GI and colonic transit times. The higher motility in the absence of D2R indicated a physiologically relevant inhibitory effect of DA on gut motility.
Gastroparesis syndromes: emerging drug targets and potential therapeutic opportunities
Published in Expert Opinion on Investigational Drugs, 2023
Le Yu Naing, Matthew Heckroth, Prateek Mathur, Thomas L Abell
Therapies for gastroparesis syndromes beyond dietary changes have focused on medications that improve symptoms and, in some cases, gastric emptying. While focusing on gastric emptying is understandable, an uneven correlation with GI symptoms and gastric emptying has been found [154,155]. While some patients have benefited from available, that is, approved or off-label, medications, improvement is often modest and often minimally effective. The fact that no new ‘motility’ drugs for Gp have been approved in 40 years is concerning. In addition, few, if any, available or even investigational medications can be classified as disease modifying. Since detailed investigations into GpS are still relatively new, the natural history of GpS is not well known[12]. Thus, while the current approach may not be wrong, it is not necessarily optimal. It is important to have reviewed what is currently used and what is in trials, to know how to move forward.
Naringenin modulates Cobalt activities on gut motility through mechanosensors and serotonin signalling
Published in Biomarkers, 2023
Adeola Temitope Salami, Ademola Adetokubo Oyagbemi, Moyosore Victoria Alabi, Samuel Babafemi Olaleye
The small intestine, is a part of the gastrointestinal tract responsible for nutritional absorption (from food), immunologic and endocrine functions (Denbow 2015, Mark and Bouwmeester 2017) besides motility. Motility within the small intestine enhances mixing, transit of secretions and digested contents from the stomach, and removal or ridding of ingested harmful or toxic substances not absorbed. Hunt et al. (1985) demonstrated that gastric emptying is hinged on the volume, composition, osmolality and caloric density of food ingested which is coordinated by the pyloric sphincter and duodenum activities. Mechanosensors (Alcaino et al. 2017) found along the small intestine aid these activities; examples of these include epithelial cells such as myenteric neurons, interstitial cells of Cajal, smooth muscle, enterochromaffin cells, glia, etc. The digestive system is propelled by the enteric nervous system (ENS) while gut hormones also regulate functioning of the intestine such as motility, secretion, cell proliferation, digestion and absorption (Ma and Lee 2020). Gastric emptying is regulated by its’ inhibitory and excitatory hormones which are also released from both the intestine and pancreas thus mediating or relating food intake, satiety, energy metabolism to gastric emptying (Goyal et al. 2019).
Guidelines and new directions in the therapy and monitoring of ATTRv amyloidosis
Published in Amyloid, 2022
Yukio Ando, David Adams, Merrill D. Benson, John L. Berk, Violaine Planté-Bordeneuve, Teresa Coelho, Isabel Conceição, Bo-Göran Ericzon, Laura Obici, Claudio Rapezzi, Yoshiki Sekijima, Mitsuharu Ueda, Giovanni Palladini, Giampaolo Merlini
Impaired gastric emptying symptoms (early satiety, postprandial fullness, bloating, nausea, vomiting and weight loss) can be improved with dietary changes including small-volume meals with low soluble fibre and fat content. Additionally pharmacological approach with prokinetics can be used with erythromycin (50–250 mg a day, tdi) or Domperidone (10 mg bdi) if available. On acute attacks of recurrent vomiting short courses of metoclopramide (IV or IM) with prompt electrolyte and fluid supplementation can be useful [14]. Patients with obstinate constipation may benefit from osmotic laxatives and polyethylene glycol. Newer agents such as linaclotide, lubiprostone and prucalopride can be used when laxatives have failed. Diarrhoea, continuous or alternating with constipation can be treated with monthly cycles of rifaximin on days 1–7 followed by probiotics. Additionally, antidiarrhoeal opioids, i.e. loperamide, on demand can be used. Octreotide or opium tincture can be administered to patients with chronic diarrhoea refractory to loperamide. If the treatment of diarrhoea fails, the remaining option is a stoma.