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diabetes-acute comp

acute complications-DKA, Hypoglycemia

hypoglycemia is defined as blood glucose falls to less than 70 mg/dL
hypoglycemia is caused by too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity
mild hypoglycemic symptoms SNS nervous system is stimulated, resulting in a surge of epinephrine and norepinephrine causing sweating, tremor, tachycardia, palpitation, nervousness, and hunger
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
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
first treatment of hypoglycemia 15 g of fast-acting concentrated carbohydrate
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,
treatment for hypoglycemic patients that are unconscious and cannot swallow includes injection of glucagon 1 mg either SC or IM
glucagon is a hormone produced by alpha cells of the pancreas
funtion of glucagon stimulates the liver to release glucose (through the breakdown of glycogen)
hospital or ER treatment for hypoglycemic patients who are unconscious or cannot swallow 25 to 50 mL of 50% dextrose in water (D50W)
these patients may not experience typical symptoms of hypoglycemia patients with autonomic neuropathy, patients taking beta blockers
after administration of D50W, how long will it take hypoglycemic patient to show its effects within minutes
side affects of D50W headache, pain at injection site
3 main clinical features of DKA hyperglycemia, acidosis, and dehydration and electrolyte loss
in DKA, body attempts to get rid of excess glucose by excretion of glucose along with water and electrolytes via the kidneys
excessive urination leads to dehydration and marked electroyte loss
without insulin, the amount of glucose entering cells is reduced
without insulin, production and release of glucose by the liver is increased
in DKA, the lack of insulin allows excessive production of ketone bodies (insulin would normally prevent this from occuring)
accumulation of ketone bodies in the circulaiton leads to metabolic acidosis
3 main causes of DKA decreased or missed dose of insulin, illness or infection, and undiagnosed untreated diabetes
in response to physical and emotional stressors, there is an increase in the release of what hormones glucagon, epinephrine, norepinephrine, cortisol, and growth hormone
clinical manifestation of DKA due to hyperglycemia polyuria, polydipsia, blurred vision, weakness, headache, orthostatic hypotension, weak/rapid pulse
clinical manifestations of DKA due to detosis and acidosis anorexia, N/V, abdominal pain, fruity smelling breath, hyperventilation (Kussmaul respirations)
DKA blood glucose levels 300-800 mg/dL (some higher, some lower)
DKA bicarbonate level 0-15 mEq/L (low)
dehydration will coincide with increased levels of creatinine, BUN, and hematocrit
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
rehydration effects on K decreased serum K (due to increased plasma volume), increased urinary excretion of K
reversing acidosis in DKA IV insulin infused slowly and continuously until SC insulin may be resumed, hourly glucose levels
nursing care of patients with DKA includes monitoring fluid, electolyte, and hydration status, blood glucose levels, urine output, vital signs, breath sounds, ABGs,
nursing care of patients with DKA includes administering 1st- fluids, insulin, and other meds
DKA onset is rapid (less than 24 hrs)
HHNS onset is slow (over several days)
DKA is usually seen in type I diabetics
HHNS is usually seen in type II diabetics
DKA precipitated by omission of insulin, physiologic stress (infection, surgery, CVA, MI)
HHNS precipitated by physiologic stress (infection, surgery, CVA, MI)
HHNS blood glucose levels greater than 600 mg/dL
HHNS pH and bicarbonate levels normal
clinical manifestations of HHNS hypotension, profound dehydration, tachycardia, altered sensorium, seizures, hemiparesis
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)
treatment of HHNS fluid replacement, correction of electrolyte imbalances, and insulin administration
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
Created by: melissalouise
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