Term
| what is a normal blood glucose? |
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Definition
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Term
| what is A1C? when would its levels be high? |
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Definition
| A1C: glycated hemoglobin, high levels of which correlate w/high blood glucose |
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Term
| what happens at a glucose level of 30-60? |
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Definition
| pts at this level will seize, become unresponsive and die |
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Term
| what is the problem with correcting extreme hyperglycemia (1800) too quickly? |
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Definition
| b/c glucose is osmotically active, it will, in high amounts pull more fluid into the vasculature. if the hyperglycemia is corrected too quickly, this extra fluid will shift quickly back to the extracellular space = edema, and possibly death. |
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Term
| what are the 2 kinds of DM? |
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Definition
| DM type I: juvenile/insulin-dependent DM and DM type II: adult onset DM |
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Term
| what is the etiology of DM type I? |
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Definition
| immunologic destruction (possibly virally-related) of pancreatic islet beta cells = *little/no insulin production. this is also referred to as: IDDM (insulin dependent diabetes mellitus) |
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Term
| what is the etiology of DM type II? |
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Definition
| there is a *diminished response to insulin, meaning adequate amounts of insulin exist - but there is a problem with the receptors (problems binding or downregulation). *obesity helps to diminish the response of insulin, possibly via counter-hormones, certain estrogenic products and blood flow variation. pts at *ages > 40 are more also more likely to develop a diminished response to insulin. this is also referred to as: NIDDM (non-insulin dependent diabetes mellitus) |
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Term
| how does DM cause keto-acidosis? |
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Definition
| the body is hyperglycemic, but not enough of that glucose is getting into cells, and since the body still needs fuel - it switches to beta oxidation: burning of lipids to produce ketones. these ketones produce acidemia which then places additional stress on the body. |
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Term
| what characterizes the normal transport of insulin into cells? |
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Definition
| when insulin binds to cell membranes, it causes a stoichiometric change - allowing glucose to enter the cell and get to the mitochondria. K+ is also brought intracellularly in this process. |
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Term
| what changes in a pt w/no insulin or insulin tolerance? |
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Definition
| blood glucose, K+ levels rise, causing blood osmolarity to generally increase - but Na+ levels will decrease to maintain electroneutrality. ketones may become present in urine. |
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Term
| what are some of the physiologic considerations when treating a DM pt? |
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Definition
| b/c osmolarity is increased in the hyperglycemic DM pt, some of that glucose is going to be urinated out - and water will follow it = dehydration, hyponatremia, hypokalemia, hyperglycemia. if fluids are given along w/insulin then the GFR will also increase, so this has to be done slowly so that all the glucose isn't simply filtered out by the kidneys. K+, Na+, Mg and phos levels need to also be monitored/maintained. a compensatory respiratory alkalosis may also occur due to the metabolic acidosis caused by ketone levels in this state (monitor changes). if glucose levels get too high (8-900): coma. |
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Term
| what is the tx strategy for type I DM pts? |
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Definition
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Term
| what is the tx strategy for type II DM pts? |
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Definition
| oral hypoglycemic agents (potentiate insulin/inhibit breakdown), dietary modification, manage electrolytes, and encourage exercise |
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Term
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Definition
| < 50 mg/dl, which can be lethal faster than hyperglycemia (have to be careful not to overtreat hyperglycemia) |
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Term
| how much glucose is needed per kg for normal function? |
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Definition
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Term
| what is the recommended amount of carbs intake per day? |
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Definition
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Term
| what are DM pts at a great risk for developing? |
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Definition
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Term
| what are the various etiologies for hypoglycemia? |
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Definition
| excess insulin, excess oral hypoglycemic dosing/intake (may be long-acting), change in oral intake, change in activity, disease process, medication changes (other meds may interact w/glucose metabolism), surgery (esp if NPO preop), pentamidine, ASA, haloperidol, age extremes, insulinoma, renal failure, adrenal insufficiency, sepsis, ETOH, and heart failure. |
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Term
| how do pts w/hypoglycemia present? |
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Definition
| sweating/diaphoretic, trembling (irritable/nervous), light-headedness, palpitations, irritability, lack of focus/confusion, seizures and focal neurological deficits |
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Term
| what is tx for hypoglycemic pts? |
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Definition
| glucose IV amp D50, and if unresponsive, another administration. if no IV available/renal problems: glucagon 1-2 mg IM. monitor/maintain fluids and electrolytes. |
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Term
| when should hypoglycemic pts be admitted? |
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Definition
| if their mental status changes, if they are unable to function, if their glucose levels are unstable, if they have taken a long-acting insulin/oral hypoglycemic agent, if they cannot tolerate PO tx, if they are suicidal, and if there are co-morbid factors. |
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Term
| what characterizes hyperglycemia? |
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Definition
| blood glucose levels > 80-120 mg/dl, (but may not have to tx until 140-150). also look at HA1C and ketone levels. |
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Term
| what other diseases does DM/obesity increase the risk of? |
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Definition
| heart disease, stroke (damage to vasculature/smooth muscle/plaque formation), kidney disease (damage to glomeruli), nerve disease (secondary to glycosylation of nerve terminals), eye disease, and CA/alzheimer's |
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Term
| what are the physiologic consequences of hyperglycemia? |
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Definition
| osmotic diuresis (put out more fluid AND particles), electrolyte imbalance (pseudohyponatremia secondary to hyperglycemia/kalemia), impairment of WBCs (increased risk of sepsis), retinopathy, neuropathy (often unknown foot damage), CAD/CVA, PVD (peripheral vascular disease), and ketoacidosis (can kill) |
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Term
| can DM potentiate atherosclerotic plaques? |
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Definition
| yes, if in coronary: MI, if in brain: stroke |
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