ORALBOARDPREPARATIONPATHOPHYSIOLOGY

ORALBOARDPREPARATIONPATHOPHYSIOLOGY - ORAL BOARD...

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Unformatted text preview: 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 bcuz 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 bcuz 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 dysrhythmias-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). ***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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This note was uploaded on 03/25/2010 for the course PAR 100 taught by Professor Alan during the Spring '10 term at Miramar College.

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ORALBOARDPREPARATIONPATHOPHYSIOLOGY - ORAL BOARD...

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