sustained several fractures and a ruptured spleen

Discussion in 'MRCS Forum' started by Lona., Dec 20, 2007.

  1. Lona.

    Lona. Guest

    If blood and serum assays were gathered from a 70-yrs-old man who sustained several fractures and a ruptured spleen after fall from 20 ft. they wound demonstrates-
    a- Decreased liver gluconeogenesis
    b- Inhibition of skeletal muscle breakdown by interleukin 1 and tumor necrosis factor (TNF, cachectin)
    c- Decrease urinary nitrogen loss
    d- Hepatic synthesis if acute phase reactions
    e- Decreased glutamine consumption by fibroblasts, lymphocytes and intestinal epithelial cells
  2. Lona.

    Lona. Guest

    Answer: d. (Weissman, anesthesiology 73:308-327, 1990) Injury and sepsis result in accelerated protein breakdown with increased urinary nitrogen loss and increased peripheral release of amino acids. The negative nitrogen balance represents the net result of breakdown and synthesis (with breakdown increased and synthesis increased or diminished). Amino acids such as alanine are released by muscle and transported to the liver for incorporation into acute-phase proteins including fibrinogen, complement, heptoglobin and ferritin. The amino acids also undergo gluconeogenesis to glucose, which is utilized primarily by the brain and other glycolytic tissues such as peripheral nerves, erythrocytes, and bone marrow. Other tissues receive energy from fat in the form of fatty acids or ketone bodies during starvation following major trauma; this helps to conserve body protein. Glutamine is the most abundant amino acid in the blood, and its levels in muscle and blood decrease following injury and sepsis as it is consumed rapidly by replicating fibroblasts, lymphocytes, and intestinal endothelial cells. The use of glutamine may decrease protein catabolism in the intestine and may help prevent atrophy of the gastrointestinal tract in starved and parenterally nourished patients. Along with the counterregulatory hormones (glucagon, epinephrine, cortisol), interleukin 1 appears to mediate muscle breakdown. Recent studies have indicated that TNF (also called cachectin because of the role it plays in muscle wasting in septic or oncologic patients) also may be a principal catabolic cytokine in the traumatized patient. This protein is secreted by macrophages and further affects metabolism by inducing secretion of interleukin 1 and inhibiting synthesis and activity of lipogenic enzymes.

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