Insulin & Diabetic Emergencies

Insulin & Diabetic Emergencies

1. Diabetes mellitus — definition & relevance to insulin therapy

• Diabetes mellitus (DM) is a heterogeneous spectrum of metabolic disorders sharing impaired glucose homeostasis and hyperglycaemia, arising from some combination of insufficient insulin secretion, reduced responsiveness to insulin, increased glucose production, and abnormal fat/protein metabolism (G&G 14e Ch.51, p.1023).
• KDT's working definition: fasting plasma glucose ≥126 mg/dL and/or ≥200 mg/dL 2 h after 75 g oral glucose, with glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia (KDT 8e Ch.19, p.280).
• Chronic morbidity is from end-organ damage — retinopathy, neuropathy, nephropathy (microvascular) and cardiovascular disease (macrovascular); mitigated by sustained glycaemic control (DCCT/EDIC) (G&G 14e Ch.51, p.1023).
• Diagnostic thresholds (ADA/WHO, Table 51-1 / 41-4): symptoms + random glucose ≥11.1 mM (200 mg/dL); OR fasting ≥7.0 mM (126 mg/dL); OR 2-h OGTT ≥11.1 mM (200 mg/dL); OR HbA₁c ≥6.5% (G&G 14e Ch.51, p.1027; Katzung 16e Ch.41, p.790).
• HbA₁c reflects non-enzymatic glycation of haemoglobin over the preceding ~8–12 weeks (2–3 months); fructosamine (glycosylated serum proteins) reflects ~2 weeks (G&G 14e Ch.51, p.1030; KDT 8e Ch.19, p.281).
• Type 1 (IDDM, juvenile onset): autoimmune (type 1A, β-cell antibodies present) or idiopathic (type 1B) β-cell destruction → absolute/near-total insulin deficiency; ~5–10% of diabetes; ketosis-prone; insulin mandatory (G&G 14e Ch.51, p.1028; KDT 8e Ch.19, p.280).
• Type 2 (NIDDM, maturity onset): >90% of cases; combination of insulin resistance (liver, muscle, fat) and relative β-cell insufficiency; obesity in ~80%; strong genetic component (G&G 14e Ch.51, p.1028; KDT 8e Ch.19, p.281).
• Latent autoimmune diabetes of adults (LADA): up to 10–15% of phenotypic "type 2" patients have a milder, indolent autoimmune (type 1) process and eventually need insulin (Katzung 16e Ch.41, p.789).
• Other forms: monogenic (MODY — HNF1A/HNF4A/glucokinase; MODY-3 responds to sulfonylureas), neonatal diabetes (KATP/insulin-gene mutations), pancreatic disease, endocrinopathies, drug-induced (glucocorticoids, atypical antipsychotics, calcineurin/mTOR inhibitors, protease inhibitors), gestational DM (G&G 14e Ch.51, p.1030; KDT 8e Ch.19, p.281).