Nr 507 week 5 discussion (parts 1, 2, 3) + quiz answers
At a molecular level, ketoacidosis develops due to several key processes taking place within the body . First , free fatty acids (FFA) are released from adipose tissue into circulation – providing substrates for hepatic & peripheral oxidation – resulting in increased production of acetyl-CoA molecules . Secondly , acetyl-CoA enters mitochondria where it undergoes beta-oxidation leading to further elevation of these molecules & their derivatives (acetoacetate & beta hydroxybutyrate ) . Further metabolism by enzymes such as thiophorase results in decreased citrate concentrations which inhibit ATP synthesis thus limiting glucose uptake/utilization ability while simultaneously promoting glycogenolysis & gluconeogenesis ultimately leading to hyperglycemia & subsequent acidification through generation of H+ ions via lactate dehydrogenase enzyme activity.
In summary , without proper regulation through insulin release there is disruption between glucose regulation & energy availability causing large accumulation of ketone bodies within blood vessels – raising their acidity levels beyond normal range at which point we diagnose someone with ketoacidosis.