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ORAL BOARD PREPARATION PATHOPHYSIOLOGY 1. OSMOTIC DIURESIS : DEFINITION: OSMOTIC DIURESIS- greatly increased urination and dehydration caused when high levels of glucose CANNOT be reabsorbed into the blood (180mg/dL) from the kidney tubules and the osmotic pressure of the glucose in the tubules prevents water reabsorption dehydration. SO… - normally when the kidneys filter blood in the glomeruli- reabsorb useful materials (water, glucose…) -glucose is normally reabsorbed into the body through an active transport process -the body tries to regulate blood glucose between 80-140mg/dL (homeostasis body balanced and happy) -kidneys trying to excrete glucose when 180+ mg/dL (to prevent acidosis) – glucose pulls out fluids with it b’cuz it hypertonic when compared to blood increase in urine (polyuria) CAUSED BY: -if glucose levels are above 180mg/dL, glucose is excreted in the urine and pulls water out with it b’cuz osmotic pressure rises in the kidney and is hypertonic to blood- (osmotic pressure makes water follow glucose in urine). S/S: polyurea(urine, much- pee a lot) diuresis (formation and secretion of large amounts of urine)- glycosuria (glucose in urine, sweet urine – ‘mellitus’) -if this flow rate inside the kidney increases it may cause increased excretion of potassium hypokalemia, which may cause cardiac dysrhythmia’s -usually occurs in diabetes type I Rx: -fluids -insulin as indicated 2. DKA vs HHNK DEFINITION: DKA -diabetic ketoacidosis- complication of TYPE I diabetes due to decreased insulin intake. Marked by high blood glucose, metabolic acidosis, and, in advanced stages, coma (diabetic coma).
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***TYPE 1 DM -(very low or no insulin production in the body) CAUSED BY : -profound insulin deficiency and increased glucagon (pancreatic hormone signals release of glycogen- store sugar) activity -noncompliance with insulin injections -physiological stress/serious infection – (sympathetic response) causes release of catecholamines (epi, norepi, dopamine) –potentiating glucagons effects/blocks insulin effects -insufficient insulin to allow glucose into cells body compensates – gluconeogenesis- switches from glucose to fat based metabolism as energy source -ketone bodies- 3 products produced by the catabolism of fatty acids: -acetoacetic acid -beta hydroxybutyric acid -acetone -ketosis the presence of significant quantities of ketone bodies in the blood -blood level of ketone rises acidosis 7.4pH 6.0pH sugars could be 300mg/dL+ -slow onset 12-24hours -S/S : -polyurea, polydipsia, polyphagia -Kussmaul Resps - ↑rate and depth -warm/dry skin and mucos membranes -fruity odor on breath -nausea/vomiting -fever (if infection) -abd pain -↓ LOC -tachycardia -electrolyte abnormalities/ hyperglycemia -↑ pulse ↓BP -dim vision -Rx : -fluids -insulin as directed HHNK DEFINITION -Hyperglycemic Hyperosmolar Nonketotic Coma- TYPE II DM -complication of type II diabetes -dehydration -inadequate insulin activity -decreased LOC.
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