الفهرس 
GASTROINTESTINAL TRACT ANATOMYOnly 14 pages are availabe for public view
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Abstract
The gastrointestinal (GI) tract consists of the mouth, pharynx, oesophagus, stomach, duodenum, jejunum, small and large intestines, rectum and anal canal. It is a muscular tube, approximately 9m in length, and it is controlled by the autonomic nervous system. The GI tract is responsible for the breakdown, digestion and absorption of food, and the removal of solid waste in the form of faeces from the body. As food is eaten, it passes through each section of the GIT and is subjected to the action of various digestive fluids and enzymes.
In the critically ill, motility of the entire gastrointestinal tract may be affected. The tone of the lower oesophageal sphincter was markedly reduced and is likely to increase the propensity for gastro-oesophageal reflux. In patients that are sedated and ventilated, reflux is regarded as a major cause of aspiration, and consequent ventilator-associated pneumonia.
Absorption of nutrient is substantially impaired in the critically ill. The altered absorption may be a consequence of disordered transit of chyme and/or impaired mucosal function. In addition, the epithelial barrier function is impaired, with a consequent increase in gastrointestinal permeability, and a potential predisposition to translocation of enteric organisms, systemic infection and, hence, adverse outcomes.
Hyperglycaemia is common in acute illness, even in those patients without pre-existing diabetes. marked hyperglycaemia (blood glucose >12 mmol/l) is associated with poor outcomes in intensive care unit patients. Substantial hypoglycaemia (blood glucose <2.2 mmol/l) occurred frequently with intensive insulin therapy, and hypoglycaemia is also associated with adverse outcomes. Hence, while the optimum blood glucose target in the critically ill remains uncertain, treatment of hyperglycaemia and avoidance of iatrogenic hypoglycaemia are priorities. Moreover, there is evidence that glycaemic variability, in addition to mean glucose, is deleterious. Safer methods for the management of hyperglycaemia in the critically ill are therefore desirable.
In health, peptides released from the stomach and/or intestine modulate motility, secretion, absorption, mucosal growth and immune function of the gastrointestinal tract. These hormones also have effects outside the gastrointestinal tract, particularly in relation to the regulation of energy intake and glycaemia. In critically ill patients, both the prevalence and magnitude of disordered gastrointestinal and metabolic function are substantial. Moreover, many of these abnormalities are associated with poor outcomes. It is now apparent that a number of gastrointestinal hormones mediate, or have the potential to mediate, some of the functional abnormalities that occur in the critically ill, either via increased or decreased secretion.
Treating disordered hormone secretion (with manipulation of endogenous secretion, specific antagonists, exogenous infusion of hormones, or their analogues) represents a novel therapeutic approach that warrants evaluation, and has the potential to lead to improved outcomes in critically ill patients.