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1) DKA is more common in Type 1 2) HHS is more common in Type 2 3) DKA a) Triad of symptoms i) Hyperglycemia (1) Absolute insulin deficiency, so glucose doesn’t go into the cells, resulting in hyperglycemia. (2) Lack of glucose in cells causes the body to think it is hypoglycemic, so there is increased gluconeogenesis by the liver. (main cause) ii) Ketogenesis (1) Because the body thinks it is hypoglycemic, it releases fasting state hormones (glucagon, catecholamines, cortisol, ACTH, GH, etc) (2) Epinephrine causes adipose to release FFA (3) Increase in FFA causes the liver to increase ketogenesis iii) Acidosis (1) Increased ketone bodies deplete HCO3 in the body, resulting in acidosis. b) Lab findings i) Plasma glucose >250 ii) Low pH, low HCO3 iii) Urine and serum ketones iv) Anion gap >12 v) Very low C-peptide c) Clinical findings i) Polyuria, polydipsia, polyphagia ii) Weight loss despite increased appetite. iii) Hyperlipidemia – due to conversion of FFA to VLDL. iv) Kussmaul breathing – deep, rapid, labored breaths 4) HHS a) Symptoms i) Hyperglycemia (1) Relative insulin deficiency so increased glycogenolysis and decreased glucose utilization. (2) Body thinks its hypoglycemic, so increased gluconeogenesis. ii) Hyperosmolarity (1) Hyperglycemia causes osmotic diuresis (glycosuria), which leads to dehydration and hyperosmolarity. b) Lab findings i) Plasma glucose >600 ii) Serum osmolarity >320 c) Clinical findings i) Few ketone bodies – because enough insulin action to prevent lipolysis. 5) Points from lecture a) Major cause of bother DKA and HHS is infection i) Infection is more common of a cause in HHS. ii) Pneumonia is most common b) Hormone of fed state is insulin c) Hormone of fasting state is glucagon d) Stress can cause hyperglycemia that messes up any test. e) Death from these is due to fluid loss leading to circulatory failure. f) Insulin deficiency causes increased BUN due to protein breakdown. g) Gluconeogenesis uses the AA Alanine h) Increased FFA from lipolysis and AA from proteinolysis in the liver both trigger gluconeogenesis. i) FFA’s are central to development of DKA i) FFA inhibits glycolysis ii) FFA increases fatty acyl Coa, which inhibits the TCA cycle. j) Diabetic DKA i) Increased gluconeogenesis ii) Increased keogenesis iii) Increased lipolysis iv) Decreased glycolysis k) Treatment i) Diabetic ketoacidosis causes reduced fluid volume ii) First treatment is isotonic saline to restore volume iii) Then switch to hypotonic saline to increase intracellular volume.
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