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Dabietes mallotus

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diabetes mellitus overview types classification pathophysiology 2025

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Diabetes Mellitus

(Note: "Dabietes mallotus" is interpreted as Diabetes Mellitus - a common spelling variation.)

Definition

Diabetes mellitus (DM) is a metabolic disease characterized by elevated blood glucose (hyperglycemia) resulting from absent or inadequate pancreatic insulin secretion, with or without concurrent impairment of insulin action. - Katzung's Basic and Clinical Pharmacology, 16e

Classification (ADA - 4 Types)

The American Diabetes Association (ADA) classifies DM into four clinical types:
TypeMechanism
Type 1 DM (T1DM)Autoimmune beta-cell destruction → absolute insulin deficiency
Type 2 DM (T2DM)Progressive loss of beta-cell insulin secretion + insulin resistance
Gestational DM (GDM)Diabetes first diagnosed during pregnancy, not pre-existing
Other specific typesMonogenic (MODY, neonatal), pancreatic disease, drug-induced (steroids, antiretrovirals), post-transplant
  • Creasy & Resnik's Maternal-Fetal Medicine, Katzung's Basic and Clinical Pharmacology

Type 1 Diabetes Mellitus

  • Mechanism: Selective autoimmune beta-cell destruction in the islets of Langerhans leading to severe or absolute insulin deficiency
  • Subtypes: Type 1a (immune-mediated) and Type 1b (idiopathic)
  • Age: Most often <30 years, but can occur at any age
  • Autoantibodies present at diagnosis:
    • Anti-GAD65 (glutamic acid decarboxylase)
    • Insulin autoantibody (IAA)
    • Anti-IA2 (tyrosine phosphatase)
    • Anti-ZnT8 (zinc transporter 8)
  • Genetics: >60 genetic loci identified; highest incidence in Northern Europeans and Sardinians
  • Treatment: Parenteral insulin is essential to sustain life and prevent diabetic ketoacidosis (DKA)
  • LADA: Up to 10-15% of apparent "type 2" patients in Northern Europeans actually have latent autoimmune diabetes of adulthood (LADA), a slow-onset form of T1DM
A notable recent advance: Teplizumab (anti-CD3 monoclonal antibody) is now approved for high-risk Stage 2 T1DM patients (age ≥8) to delay onset of overt T1DM by ~25 months.
  • Katzung's Basic and Clinical Pharmacology, 16e

Type 2 Diabetes Mellitus

  • Mechanism: Tissue insulin resistance + relative insulin secretory deficiency
  • Endogenous insulin is enough to prevent ketoacidosis, but not enough to prevent hyperglycemia
  • A patient may have predominantly resistance or predominantly secretory failure
  • Initial management: Diet, exercise, and oral/injectable non-insulin agents
  • Later stages: Progressive beta-cell failure may eventually require insulin therapy
  • Katzung's Basic and Clinical Pharmacology, 16e

Diagnosis (Non-Pregnant Adults)

Any ONE of the following criteria:
  • Fasting plasma glucose ≥ 126 mg/dL (after ≥8 hours fasting)
  • 2-hour plasma glucose ≥ 200 mg/dL during 75g OGTT
  • HbA1c ≥ 6.5%
  • Random plasma glucose ≥ 200 mg/dL in a symptomatic patient

Complications

CategoryExamples
MicrovascularDiabetic nephropathy, retinopathy, neuropathy
MacrovascularCoronary artery disease, stroke, peripheral arterial disease
Acute metabolicDKA (Type 1), Hyperosmolar hyperglycemic state (Type 2), hypoglycemia

Key Treatments Summary

Type 1: Insulin (basal-bolus regimen)
Type 2 (selected drugs):
  • Metformin (first-line)
  • GLP-1 receptor agonists (e.g., semaglutide)
  • SGLT-2 inhibitors (e.g., empagliflozin)
  • DPP-4 inhibitors (e.g., sitagliptin)
  • Insulin (when needed)
Insulin types available:
  • Rapid-acting: Lispro, Aspart, Glulisine
  • Short-acting: Regular insulin
  • Long-acting (basal): Glargine, Detemir, Degludec
  • Katzung's Basic and Clinical Pharmacology, 16e
For current ADA guidelines, the 2025 ADA Standards of Care are the most up-to-date reference.
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