acute complications-DKA, Hypoglycemia
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| hypoglycemia is defined as | blood glucose falls to less than 70 mg/dL
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| hypoglycemia is caused by | too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity
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| mild hypoglycemic symptoms | SNS nervous system is stimulated, resulting in a surge of epinephrine and norepinephrine causing sweating, tremor, tachycardia, palpitation, nervousness, and hunger
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| moderate hypoglycemic symptoms | impaired CNS function: inability to concentrate, headache, lightheadedness, confusion, memory lapses, numbness of the lips and tongue, slurred speech, impaired coordination, emotional changes, irrational or combative behavior, double vision, drowsiness
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| severe hypoglycemic symptoms | impairment of CNS function so severe that patient needs assistance of another person for treatment, disoriented behavior, seizures, difficulty arousing from sleep, or loss of consciousness
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| first treatment of hypoglycemia | 15 g of fast-acting concentrated carbohydrate
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| examples of 15 g fast-acting carb | 3-4 commercially prepared glucose tablets, 4-6 oz of fruit juice, regular soda, or milk, 6-10 hard candies, 2-3 teaspoons of sugar or honey,
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| treatment for hypoglycemic patients that are unconscious and cannot swallow includes | injection of glucagon 1 mg either SC or IM
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| glucagon is | a hormone produced by alpha cells of the pancreas
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| funtion of glucagon | stimulates the liver to release glucose (through the breakdown of glycogen)
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| hospital or ER treatment for hypoglycemic patients who are unconscious or cannot swallow | 25 to 50 mL of 50% dextrose in water (D50W)
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| these patients may not experience typical symptoms of hypoglycemia | patients with autonomic neuropathy, patients taking beta blockers
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| after administration of D50W, how long will it take hypoglycemic patient to show its effects | within minutes
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| side affects of D50W | headache, pain at injection site
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| 3 main clinical features of DKA | hyperglycemia, acidosis, and dehydration and electrolyte loss
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| in DKA, body attempts to get rid of excess glucose by | excretion of glucose along with water and electrolytes via the kidneys
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| excessive urination leads to | dehydration and marked electroyte loss
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| without insulin, the amount of glucose entering cells | is reduced
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| without insulin, production and release of glucose by the liver | is increased
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| in DKA, the lack of insulin allows excessive production of | ketone bodies (insulin would normally prevent this from occuring)
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| accumulation of ketone bodies in the circulaiton leads to | metabolic acidosis
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| 3 main causes of DKA | decreased or missed dose of insulin, illness or infection, and undiagnosed untreated diabetes
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| in response to physical and emotional stressors, there is an increase in the release of what hormones | glucagon, epinephrine, norepinephrine, cortisol, and growth hormone
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| clinical manifestation of DKA due to hyperglycemia | polyuria, polydipsia, blurred vision, weakness, headache, orthostatic hypotension, weak/rapid pulse
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| clinical manifestations of DKA due to detosis and acidosis | anorexia, N/V, abdominal pain, fruity smelling breath, hyperventilation (Kussmaul respirations)
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| DKA blood glucose levels | 300-800 mg/dL (some higher, some lower)
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| DKA bicarbonate level | 0-15 mEq/L (low)
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| dehydration will coincide with increased levels of | creatinine, BUN, and hematocrit
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| rehydration for DKA patients includes | 0.9% sodium chloride for 1st 2-3 hours, half-strength (45%) normal saline after 1st few hours, dextrose 5% in water (D5W) after glucose reaches 300 or less
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| rehydration effects on K | decreased serum K (due to increased plasma volume), increased urinary excretion of K
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| reversing acidosis in DKA | IV insulin infused slowly and continuously until SC insulin may be resumed, hourly glucose levels
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| nursing care of patients with DKA includes monitoring | fluid, electolyte, and hydration status, blood glucose levels, urine output, vital signs, breath sounds, ABGs,
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| nursing care of patients with DKA includes administering | 1st- fluids, insulin, and other meds
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| DKA onset is | rapid (less than 24 hrs)
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| HHNS onset is | slow (over several days)
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| DKA is usually seen in | type I diabetics
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| HHNS is usually seen in | type II diabetics
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| DKA precipitated by | omission of insulin, physiologic stress (infection, surgery, CVA, MI)
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| HHNS precipitated by | physiologic stress (infection, surgery, CVA, MI)
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| HHNS blood glucose levels | greater than 600 mg/dL
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| HHNS pH and bicarbonate levels | normal
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| clinical manifestations of HHNS | hypotension, profound dehydration, tachycardia, altered sensorium, seizures, hemiparesis
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| HHNS pathophysiology | insulin level is too low to prevent hyperglycemia (and subsequent osmotic diuresis) but it is high enough to prevent fat breakdown (preventing ketosis and acidosis)
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| treatment of HHNS | fluid replacement, correction of electrolyte imbalances, and insulin administration
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| HHNS fluid treatment | 0.9% or 0.45% NS, K is added to IV fluids when UOP is adequate, insulin administered at a continuous low rate, IV fluids with dextrose are administered after glucose decreases to 250-300 mg/dL
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