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Diagnosis of diabetes is made by a random glucose level ≥200 mg/dL with concurrent symptoms of hyperglycemia (blurry vision, thirst, polyuria, weight loss) or any two of the following tests performed on the same day or any one of the following tests performed on different occasions:
Fasting blood glucose level (after 8-hour fasting) ≥126 mg/dL
Oral glucose tolerance test (highest sensitivity)—8-hour fasting, followed by drinking 75 g glucose; check blood glucose 2 hours later, glucose level ≥200 mg/dL
Hemoglobin A1c level ≥6.5 % (lowest sensitivity)
Impaired glucose tolerance (prediabetes) is diagnosed by fasting blood glucose between 110 and 125 mg/dL or oral glucose tolerance test between 140 and 200 mg/dL.
Type 1 diabetes (5%–10% of total) is caused by autoimmune destruction of beta cells in the islets of Langerhans; insulin supplementation is required.
Type 2 diabetes (90%–95% of total) is caused by a combination of peripheral insulin resistance and relative insulin deficiency; it is treated by weight loss, diet modification, oral agents, or insulin.
Diagnosis is made by possessing any three of the following traits:
Serum triglycerides ≥150 mg/dL or treatment for high triglycerides
High-density lipoprotein (HDL) less than 40 mg/dL in men or less than 50 mg/dL in women, or treatment for low HDL
Abdominal obesity (waist circumference ≥102 cm in men or ≥88 cm in women)
Blood pressure ≥130/85 mm Hg, or treatment for hypertension
Fasting blood glucose greater than 100 mg/dL or treatment for hyperglycemia
Treatment involves treating the underlying cause (obesity) and cardiovascular risk factors (lipid-lowering agents and antihypertensive therapy).
Sulfonylureas (glipizide [Glucotrol], chlorpropamide, glimepiride, glyburide, tolazamide, tolbutamide)—stimulate insulin release from beta cells by inhibiting the adenosine triphosphate (ATP)-dependent potassium channel in the pancreatic beta cells
Can cause hypoglycemia (notably glyburide and chlorpropamide) and weight gain
Short-acting insulin secretagogues (repaglinide [Prandin], nateglinide)—similar mechanism to sulfonylureas, shorter acting; less risk for hypoglycemia
Thiazolidinediones (pioglitazone [Actos], rosiglitazone)—increase peripheral insulin sensitivity by binding to peroxisome-proliferator-activated receptor gamma in the nucleus, which alters DNA transcription
Can cause edema and weight gain and induce heart failure
Biguanides (metformin [Glucophage])—decrease hepatic glucose production by suppressing gluconeogenesis (inhibits mitochondrial glycerophosphate dehydrogenase) and increase insulin sensitivity in peripheral tissue
Less hypoglycemia than sulfonylureas
Higher risk for lactic acidosis and may cause gastrointestinal upset; contraindicated in renal failure, hepatic dysfunction, congestive heart failure (CHF), metabolic acidosis, alcoholism, and dehydration
Hold before administration of intravenous (IV) contrast, in acute illness, and surgery.
α-Glucosidase inhibitors (acarbose [Precose], miglitol)—delayed glucose absorption from intestine by competitive inhibition of α-glucosidase
Can cause flatulence, abdominal discomfort, and diarrhea
Dipeptidyl peptidase 4 (DPP-4) inhibitors (sitagliptin [Januvia], saxagliptin, linagliptin, alogliptin)—inhibit DPP-4, resulting in prolonged glucagon-like peptide-1 levels and increased insulin synthesis
Glucagon-like peptide receptor agonists (liraglutide [Victoza], albiglutide, dulaglutide)—similar mechanism to DDP-4 inhibitors; not considered initial therapy
Rapid-acting—lispro (Humalog), aspart (NovoLog)
Onset 15–30 minutes, peak 30–90 minutes, duration 3–4 hours
Used in continuous subcutaneous insulin pumps; can be given IV
Fast-acting—regular (Humulin R, Novolin R)
Onset 30–60 minutes, peak 2–4 hours, duration 6–10 hours
Used in continuous IV infusions and more immediate when IV
Intermediate-acting—NPH (Humulin N, Novolin N)
Onset 1–4 hours, peak 4–12 hours, duration 12–24 hours
Subcutaneously; cannot be given IV
Long-acting—glargine (Lantus), degludec (Tresiba), detemir (Levemir pen)
Onset 1–2 hours, peak 3–20 hours, duration 24–30 hours
Subcutaneously; cannot be given IV
Goal blood glucose varies, usually 80–130 mg/dL before meal and 90–140 mg/dL at bedtime.
Weight-based estimation of insulin need
Type 1 diabetic will require 0.4–0.7 unit/kg per day.
Type 2 diabetic will require 0.3–1 unit/kg per day.
Traditional subcutaneous sliding scale insulin
Fast- or rapid-acting insulin is dosed before every meal and at bedtime, or every 6 hours schedule for patients not eating, based on blood glucose level checked at that time.
When 24-hour insulin requirement is known, either after conversion from continuous IV infusion or after doses of subcutaneous sliding scale given for 1 day, may add long-acting insulin to regimen totaling 50%–66% of daily requirement.
Advantages include being commonly used and relatively easy to order and administer.
Disadvantages include being nonphysiologic and reactive in treating hyperglycemia.
Basal-bolus-correction subcutaneous dosing
Goal is to administer 50% of daily insulin in a long-acting form to mimic physiologic continuous basal insulin secretion and 50% as three subcutaneous boluses of fast- or rapid-acting insulin to mimic physiologic prandial insulin peaks.
Based on premeal blood glucose levels, subcutaneous “correction” dose of fast- or rapid-acting insulin may be given with scheduled bolus. Basal and bolus doses are then adjusted for the next day’s orders to try to eliminate need for correction doses.
Bolus doses are given on every 6 hours schedule for patient who is not eating and receiving continuous tube feeds.
Advantages include being more physiologic.
Disadvantages include being a more confusing regimen to order and administer.
Continuous IV insulin infusion (insulin drip)
In most hospitals, it is used only in intensive care unit (ICU) setting.
Most commonly regular insulin is used.
Target glucose is 140–180 mg/dL.
Intense glycemic control (80–110 mg/dL) has shown no survival benefit and has greater risk of hypoglycemia and greater mortality.
Blood glucose level checks are every hour to minimize hypoglycemia (associated with increased morbidity and mortality).
When transitioning from insulin infusion to subcutaneous insulin injection, there must be at least a 2-hour overlap of the infusion and injection.
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