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diabetes-acute comp
acute complications-DKA, Hypoglycemia
| Question | Answer |
|---|---|
| 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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