NSD 481 Lecture Notes - Lecture 8: Hypermetabolism, Protein Catabolism, Fluid Replacement
Document Summary
How is the metabolic response to critical illness similar to starvation. Metabolism goes up in illness starvation it goes down. Pt is nutritionally (cid:494)at risk(cid:495) when he/she is at risk for poorer outcome than if she/he was not malnourished. Three phases: ebb phase (2-48 hours, flow phase (next, recovery. Proteins in liver that are synthesized in response to injury and infection. Stimulate kidneys in order to preserve fluid and sodium retention. Get fluid and salt conservation (supports blood volume) reduction in urine output. Restore blood flow to organs; want fluid in= fluid out. Marked increase in glucose production and ffa release. High circulating levels of epi/norepi, glucagon, and cortisol. Elevated levels of (cid:498)counterregulatory(cid:499) (cid:523)raise blood sugar(cid:524) or stress hormones. Promotes gluconeogenesis, aa uptake, ureagenesis (have to get rid of nitrogen/protein), and protein catabolism. Promotes gluconeogenesis, glycogenolysis (breakdown glycogen), and acute-phase protein synthesis. All stored glucose depleted in ~24 hour all patients that are ill will develop hyperglycemia.