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DM and hypoglycemia

Endocrine Focus #3:Diabetes Mellitus and Hypoglycemia

DM and hypoglycemiaAnswer
Diabetes Mellitus:definition chronic disorder characterized by impaired metabolism and by vascular and neurologic complications
endogenous created by one's own body
exogenous comes from an external source
Type 1 DM characterized by the absence of endogenous insulin. Most commonly occurs in juveniles and young adults. Persons will require exogenous insulin for a lifetime
Type 2 DM characterized by inadequate endogenous insulin and the body's inability to properly use insulin. Beta cells respond inadequately to hyperglycemia & beta cells become desensitized to high levels of glucose in blood.
Gestational diabetes mellitus diagnosed when a woman is found to have glucose intolerance for first time during pregancy. P delivery, condition resolves.
the three P's of DM (s/s) polydipsia (excessive thirst), polyuria (excessive urine volume), and polyphagia (excessive hunger)
roles of insulin transport of glucose into resting muscle, regulates carbohydrate use, promotes fatty acid synthesis, spares fat, stimulates protein synthesis, inhibits conversion of protein into glucose, promotes conversion of glucose to glycogen/inhibit glycogen-glucose
result of lack of insulin stimulates the conversion of glycogen to glucose, permits fat stores to break down, increases triglyceide storage in the liver, halts the storage of proteins, and causes protein to be dumped into the bloodstream
Type 1 DM:etiology attributed to genetic, immunologic, and environmental factors. A possible autoimmune disorder where the lympocytes and phagocytes turn on the healthy cells of the islets of Langerhans in pancreas. Islet cell antibodies found in 80% pt c dx of type 1 DM
DM type 2:risk factors Obesity, sedentary lifestyle, family hx of DM, Age 40 or >, hx of GDM, hx of delivering baby weighing >10lbs., African, Latin, or Native-American
Complications of DM retinopathy, nephropathy, macrovascular, neuropathic (mononeuropathy, polyneuropathy, & automatic neuropathy), hypoglycemic unawareness, foot complications
causes of neuropathic ulcers mechanical irritation, thermal injury, and chemical irritation
acute hypoglycemia can be triggered by taking too much insulin, not eating enough food or at the right time, and inconsistent patterns of exercise
s/s of acute hypoglycemia (adrenergic) shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or toungue, and diaphoresis.
s/s acute hypoglycemia (neuroglucopenia) drowsiness, irritability, impaired judgment, blurred vision, slurred speech, HA, and mood swings progresing to disorientation, seizures, and unconsciousness, LOC, convulsions, coma, and death
tx for hypoglycemia Give the CONSCIOUS pt 10-15 gm of quick-acting carb: 4-6 oz of undiluted OJ or apple juice or nondiet soda, 8 oz. skim milk, 3-4 tsp table sugar, 4 Tbsp corn syrup, jelly, or jam, 5-6 pieces hard candy, or 2-3 glucose tabs or 15 gm glucose gel.
diabetic ketoacidosis (DKA) a life-threatening emergency caused by a relative or absolute deficiency of insulin. This results in disorders in the metabolism of carbs, fats and protein
first 3 sequences of events in DKA 1. serum glucose levels rise. 2. The high osmotic pressure created by excess glucose leads to osmotic diuresis. As glucose is eliminated, so are large amounts of H2O and electrolytes. 3. The pt experiences polyuria.
the next 2 sequences (4-5) 4. The sympathetic nervous system responds to the cellular need for fuel by converting glycogen to glucose and manufacturing additional glucose. 5. As glycogen stores are depleted, the body begins to burn fat and protein for energy.
the last 2 sequences of DKA (6-7) 6. Fat metabolism produces acidic substances called ketone bodies that accumulate and lead to metabolic acidosis. 7. Protein metabolism results in the loss of lean muscle mass and a negative nitrogen balance
early s/s DKA anorexia, HA, fatigue, polydipsia, polyuria, and polyphagia
moderate s/s DKA dehydration, weak, lethargic, abd pain, n/v, fruity breath, inc resp rate, tachycardia, blurred vision, and hypothermia
late s/s DKA air hunger (those that are seen in Kussmaul's respirations), coma, and shock. death can result if prompt medical care is not instituted.
Lab values of pt c DKA hyperglycemia (300 mg/dL); ketonuria; and acidosis, c a pH of < 7.3 or a bicarbonate level of < 15 mEq/L
tx for DKA 1000 mL NS to run over 1st hour. 2000-8000 mL IV NS over next 24 hr. K replacements (only p adequate urine output is made.) and slow IV insulin. when glucose is @ 250-300, dextrose solution is added. IV drip is cont until bicarbonate is @ 15-18 mEq/L
Hyperglycemic hyperosmolar nonketotic syndrome (HHNKS) condition in which a pt goes into a coma from extremely high glucose levels (>600 mg/dL) but there is no evidence of elevated ketones
HHNKS:etiology pt's pancreas produces enough insulin to break down fatty acid and formation of ketones, but not enough insulin to prevent hyperglycemia. Basic defect is lack of effective insulin or the inability to use available insulin.
Dx:diabetes mellitus based on serum glucose levels. Norm fasting serum glucose levels are 80-120 mg/dL. >126 mg/dL merits further investigation. also, the 3 P's of DM, and a two-hr postprandial glucose level > 200 mg/dL, and an impaired fasting glucose test
Impaired Glucose Tolerance shows presence of moderately high glucose levels. May increase until pt has overt diabetes, decrease to norm, or remain unchanged. dx of this test is 1) fasting glucose of 110-125 mg/dL and 2) a 2-hr OGTT result 140-200 mg/dL
Oral Glucose Tolerance Test (OGTT) performed when pt suspects DM. Pt consumes 150-300 gm carbs 3 days b/4 test. night b/4, fasting is done. blood is drawn, then pt drinks glucola and blood is drawn 30min-1hr later. insert hep lock since blood will be drawn many times
exercise and the Type 1 DM pt hyperglycemia can result because insulin is inadequate. The liver may release mor glucose than metabolized and if pancreas isn't making enough insulin, the body's free fatty acids begin to form ketones, increasing the hazard of ketosis.
exercise and the Type 2 DM pt in pt's c type 2, exercise makes insulin receptor sites more sensitive to insulin and lowers plasma glucose levels. Much of the morbidity is caused by the arherosclerosis and puts the pt @ risk for CVA. stretching and cool-down exercises are recommended
pt teaching for exercise and DM avoid exercise when serum glucose is 250 mg/dL or greater, warm-up 5-10 min b/4, exercise shortly p eating or have a small snack if glucose is <100 mg/dL, avoid exercise @ peak of insulin, IJ insulin in abd, have food available if hypoglycemia occurs
Created by: blumchen on 2006-02-10



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