<aside> 🍬 Polyuria, nocturia, and weight loss in an adolescent with 1+ glucose on urine dipstick are suggestive of type 1 diabetes mellitus.

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• Absolute insulin deficiency is the underlying pathology of type 1 diabetes mellitus, caused by autoimmune-mediated destruction of pancreatic β cells. The resulting elevation of blood glucose levels leads to a range of symptoms, typically including polyuria, nocturia, polydipsia, and increased appetite.
• Nonspecific symptoms of fatigue, weight loss, and an increased tendency to infections (e.g., skin infections, UTIs) are also common. The symptoms usually develop within days to a few weeks or manifest suddenly with diabetic ketoacidosis. While glucosuria detected via urine dipstick is suggestive of diabetes mellitus, the diagnosis is confirmed through an oral glucose tolerance test or a random blood glucose level ≥ 200 mg/dL.
• Type 1 diabetes mellitus should always be suspected in the classic presentation of weight loss, lethargy, polydipsia, polyuria (and resulting secondary nocturnal enuresis), and glucosuria in a child. Additional signs of acute abdominal pain, nausea, Kussmaul breathing (deep and labored breathing), dehydration (dry mucous membranes), hyponatremia, hyperkalemia, and ketonuria all indicate life-threatening diabetic ketoacidosis (DKA), high anion gap metabolic acidosis.
• DKA typically occurs in patients with type 1 diabetes mellitus if undiagnosed and untreated or treatment failure. There are 3 mechanisms that lead to the decreased total body K+ in DKA. First, the insulin deficiency that constitutes type 1 diabetes causes hyperglycemia and resulting hyperosmolality. This triggers K+ to shift with water from cells into the extracellular space, leading to possible hyperkalemia and loss in urine. Next, the insulin-driven cellular uptake of K+ via the Na+/K+-ATPase is absent. Lastly, elevated extracellular H+ levels from metabolic acidosis reduce activity of the Na+-H+ antiporter. This decreases the intracellular Na+ gradient, which also lowers activity of the Na+/K+-ATPase, further increasing extracellular K+.
• So even though serum K+ can be normal or even paradoxically elevated, total body K+ is reduced. This is why it is especially important when treating DKA with insulin replacement, which reverses these mechanisms, to monitor K+ and be ready to supplement it if it falls below 5.3 mEq/L and maintain between 4 and 5 mEq/L. This will help prevent hypokalemia and fatal arrhythmias from intracellular shifting of potassium. If serum potassium is under 3.3, potassium chloride should be administered before insulin.

• Honeymoon period usually occurs in 1st 6 months after DM type 1 diagnosis
  • Because there is insulin reservoir in pancreas
  • can lead to hypoglycemic attacks
  • Treatment: decrease insulin dose
• In a patient with frequent hypoglycemic attacks during exercise, best site for insulin: abdomen

• Check serum glucose at 2 AM

Screening in T1DM

• Type 1 DM commonly associated with
  • Hypothyroidism (Hashimoto): Increase weight and decrease height
  • Celiac disease: Decrease weight and height
• Annual screening for urine microalbuminuria for diabetic nephropathy after 5 years from diagnosis