Lecture 35 Hyperglycemia.docx

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Michael Baker

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BCH210H © Lisa | Page 12 Lecture 35: Hyperglycemia  urinates a lot: polyuria  drinks a lot of fluid: polydipsia  breath smells sweet  eating a lot of sugars  hypotensive 90/60, low bp  breathing more rapidly, deeply and noisily (usu bad bc it changes pH of the blood)  body is trying to get rid of CO 2  may mean there is a problem w pH in blood and trying to compensate for that  urine has alone of glucose and ketone bodies  hyperglycemia  hyperglycemic and ketotic (ketosis)  glucose is mainly cyclized, but it can be in straight chain form as an aldehyde  its aldehyde can react w an amino group to form Schiff bases  vascular problems can result  low blood pH  acidosis  caused by ketone bodies (acids)  too little base (buffer)  high K +  hyperkalemia  should be inside cells  gives him hypotonic saline drip bc his blood is hypertonic w too many small molecules outside cells  type I found in young patients  type II in old patients, poor lifestyle, too much sugar in diet, frequent glucose spikes, and pancreas is too tired to make more insulin  type I autoimmune disease kills beta cells  type II, poor insulin release, or insulin resistance  no insulin, but he still has the antagonists adrenaline and glucagon  promote catabolism  locks body in a catabolic state  promote glycogenolysis  he probably doesn’t have a lot of glycogen  a lot of fat mobilization  loss of weight  due to lock in catabolic mode  can’t use sugar in blood bc no GLUT4 on membranes of cells (no insulin to promote that)  high rate of beta oxidation, but Krebs can’t keep pace  rise in acetyl CoA in mitochondria  starts ketogenesis, drives generation of ketone bodies (4C)  ketone bodies produce acetone, creating the smell on the breath (very volatile)  high blood glucose causes glycosylation rxns  interaction of glucose w lipids and nucleic acids  glycosylation adds glucose on hemoglobin,
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