Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Although aspiration is a relatively rare event during anaesthesia, it represent an important cause of anaesthesia related mortality and also of ventilator associated pneumonia in intensive care unit. The incidence of aspiration is markedly increased after trauma owing to the risk of recent ingestion of food, depression of consciousness and airways reflexes, and gastric stasis induced by raised sympathoadrenal tone. The factors which contribute to the likelihood of aspiration include the urgency of surgery, airways problems, inadequate depth of anaesthetic, use of the lithotomy position, gastrointestinal problems, depressed consciousness, increased severity of illness and obesity. Factors that predispose to aspiration pneumonia are: a gastric content with a pH less than 2.5 and a gastric volume of 0.4 ml kg-1; a reduction in lower oesophageal sphincter tone; a reduction of upper oesophageal sphincter tone and a not coordination between the pharyngeal muscle and the upper oesophageal sphincter tone during swallowing; and a depression of protective airway reflexes. Methods to minimize regurgitation and aspiration involve control of gastric contents (preoperative starvation is the method universal accepted), application of cricoid pressure and control of the airways.
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PMID:Gastric reflux and pulmonary aspiration in anaesthesia. 1276 74

Weight restoration is crucial for successful treatment of anorexia nervosa. Without it, patients may face serious or even fatal medical complications of severe starvation. However, the process of nutritional rehabilitation can also be risky to the patient. The refeeding syndrome, a problem of electrolyte and fluid shifts, can cause permanent disability or even death. It is essential to identify at-risk patients, to monitor them carefully, and to initiate a nutritional rehabilitation program that aims to avoid the refeeding syndrome. A judicious, slow initiation of caloric intake, requires daily management to respond to entities such as liver inflammation and hypoglycemia that can complicate the body's conversion from a catabolic to an anabolic state. In addition, nutritional rehabilitation should take into account clinical characteristics unique to these patients, such as gastroparesis and slowed colonic transit, so that measures can be taken to ameliorate the physical discomforts of weight restoration. Adjunct methods of refeeding such as the use of enteral or parenteral nutrition may play a small but important role in a select patient group who cannot tolerate oral nutritional rehabilitation alone.
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PMID:Nutritional rehabilitation: practical guidelines for refeeding the anorectic patient. 2079 56

Bornaviruses cause neurologic diseases in several species of birds, especially parrots, waterfowl and finches. The characteristic lesions observed in these birds include encephalitis and gross dilatation of the anterior stomach - the proventriculus. The disease is thus known as proventricular dilatation disease (PDD). PDD is characterized by extreme proventricular dilatation, blockage of the passage of digesta and consequent death by starvation. There are few clinical resemblances between this and the bornaviral encephalitides observed in mammals. Nevertheless, there are common virus-induced pathogenic pathways shared across this disease spectrum that are explored in this review. Additionally, a review of the literature relating to gastroparesis in humans and the control of gastric mobility in mammals and birds points to several plausible mechanisms by which bornaviral infection may result in extreme proventricular dilatation.
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PMID:The pathogenesis of proventricular dilatation disease. 2815 4