Metabolic Changes In Its Never-Ending Quest To Maintain Homeostasis

BASIC PATHOLOGY PAPER ASSIGNMENT HFS 3252 LECTURER’S NAME: DR ROCHMAN NAIM

TITLE: METABOLIC STRESS, BURN AND SURGERY AND THEIR NUTRITION THERAPY

PREPARED BY: LEONG SIM KIAN STUDENT NO.10 028112

SUBMITTED DATE: 31 MARCH 2011

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In its never-ending quest to maintain homeostasis, the human body responds to stress, physiologic or psychological, with a chain reaction that involves the central nervous system and hormones that affect the entire body. Magnitude and duration of the stress determine just how the body will react. It is important to understand metabolic changes that take place in reaction to stress, both in uncomplicated stress that is present when patients are at nutritional risk, and in more multifarious
There is decreased uptake of amino acids by muscle tissue, and increased urinary excretion of nitrogen (Figure 1-4). Some nonessential amino acids may become conditionally essential during episodes of metabolic stress. During stress, glutamine is mobilized in large quantities from skeletal muscle and lung to be used directly as a fuel source by intestinal cells. Glutamine also plays a significant role in maintaining intestinal immune function and enhancing wound repair by supporting lymphocyte and macrophage proliferation, hepatic gluconeogenesis, and fibroblast function (Figure 1-5).

Hepatic glucose production is increased and disseminated to peripheral tissues although proteins and fats are being used for energy. Insulin levels and glucose use are in fact increased, but hyperglycaemia that is not necessarily resolved by the use of exogenous insulin is present. This appears, to some extent, to be driven by an elevated glucagon to insulin ratio.

To support hyper-metabolism and increased gluconeogenesis, fat is mobilized from adipose stores to provide energy (lipolysis) as the result of elevated levels of catecholamine along with concurrent decrease in insulin production. If hyper-metabolic patients are not fed during this period, fat stores and proteins are rapidly depleted. This malnutrition increases susceptibility
It may occur following trauma, severe burns, infection, or shock and usually results from an uncontrolled inflammatory response and can progress to organ failure and death. MODS commonly begin with lung failure followed by failure of the liver, intestine, and kidney. Myocardial failure generally manifests later, but central nervous system changes can occur at any time. The pathogenesis of MODS is complex but usually results in the initiation of the stress response and release of catecholamine, producing a hyper-metabolic state in the patient. Higher levels of kcal and protein are necessary to meet increased metabolic demands. How patients are fed is also important. Early enteral feedings appear to maintain gut mucosal mass and barrier function and promote normal enterocytes’ growth in the gut. This is not possible with parenteral feedings (Table