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Diabetes Mellitus in Children

Diabetes Mellitus in Children

Diabetes Mellitus in Children

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DM Overview & Types - Sugar Rush Intro

  • Diabetes Mellitus (DM): Chronic hyperglycemia from defects in insulin secretion, action, or both.
  • Key Pediatric Types:
    • Type 1 DM (T1DM): Most common (~90%). Autoimmune β-cell destruction; absolute insulin deficiency. Often presents with DKA.
    • Type 2 DM (T2DM): ↑ incidence. Insulin resistance & relative deficiency. Strong obesity link.
    • MODY (Maturity Onset Diabetes of the Young): Monogenic (autosomal dominant). Non-ketotic.
    • Neonatal DM: Onset <6 months. Genetic defects (e.g., KCNJ11, ABCC8).

⭐ T1DM accounts for over 90% of childhood diabetes cases.

Pathophys & Clinical Picture - The Sweet Sickness

  • Pathophysiology:
    • T1DM: Autoimmune β-cell destruction → absolute insulin deficiency. HLA-DR3/DR4 link. Viral triggers.
    • T2DM: Insulin resistance & relative insulin deficiency. Obesity is a key risk factor.
  • Clinical Picture:
    • Classic "3 Ps": Polyuria, Polydipsia, Polyphagia (📌).
    • Weight loss (T1DM), fatigue, blurred vision.
    • Recurrent infections (e.g., candidiasis).
    • DKA: Common T1DM presentation (~25-40%): abdominal pain, vomiting, Kussmaul breathing, fruity breath, dehydration.
    • Acanthosis nigricans (T2DM insulin resistance marker).

⭐ DKA is the initial presentation in up to 40% of children with new-onset T1DM.

Diagnosis & Investigations - Cracking the Code

  • Suspect DM: Polyuria, polydipsia, unexplained weight loss.
  • Diagnostic Criteria (any one):
    • RPG ≥ 200 mg/dL + symptoms
    • FPG ≥ 126 mg/dL
    • 2-hr PG (OGTT) ≥ 200 mg/dL (1.75g/kg)
    • HbA1c ≥ 6.5% (📌 Caution: rapid onset)
  • Further Investigations:
    • Urine: Glucosuria, Ketonuria
    • Blood: Glucose, HbA1c
    • T1DM Markers: Autoantibodies (GAD65, IA-2, IAA, ZnT8)
    • C-peptide: ↓ T1DM, normal/↑ T2DM

⭐ DKA is the initial presentation in 20-40% of children with new-onset T1DM.

Management Principles - Sugar Control Central

  • Insulin Therapy:
    • Regimen: Basal-bolus (long + rapid-acting pre-meals) standard.
    • Dosing: Initial TDD $0.5-1 \text{ U/kg/day}$. Puberty/DKA $1-1.5 \text{ U/kg/day}$. Honeymoon $<0.5 \text{ U/kg/day}$.
  • Monitoring:
    • SMBG: 4-6x/day. Pre-meal target 90-130 mg/dL, post-meal <180 mg/dL.
    • HbA1c: Target <7.0% (ADA) / <7.5% (ISPAD), individualized.
  • DKA Management: (Flowchart below)
    • Key: Fluids, Insulin, K+ (📌 "FIK", fluids first).
    • Fluids: NS $10-20 \text{ ml/kg}$ (1hr); deficit + maintenance over 48hrs.
    • Insulin: IV Reg $0.05-0.1 \text{ U/kg/hr}$ (1-2h post-fluids).
    • K+: Add if K+ < 5.5 mEq/L & UOP.
  • Hypoglycemia:
    • Mild/Moderate: Rule of 15 (15g simple carbs, recheck BG in 15 min).
    • Severe: Glucagon IM/SC.

⭐ In DKA, start insulin 1-2h after fluids to prevent rapid osmotic shifts & cerebral edema.

Complications & Special Forms - Beyond the Basics

  • Chronic Complications:
    • Microvascular: Retinopathy, nephropathy, neuropathy. Annual screening from puberty or 5 yrs post-diagnosis.
    • Macrovascular: Accelerated atherosclerosis risk.
  • Associated Autoimmune: Thyroid disease, celiac disease.
  • Special Forms:
    • MODY: Genetic (AD), non-ketotic, family history.
    • Neonatal DM (NDM): Onset <6 months; genetic testing vital.
    • Cystic Fibrosis-Related Diabetes (CFRD): Screen annually from age 10.

⭐ NDM presenting in the first 6 months of life is unlikely to be autoimmune Type 1 DM; suspect monogenic diabetes. ​

High‑Yield Points - ⚡ Biggest Takeaways

  • Type 1 DM (autoimmune β-cell destruction) is most common in children.
  • Presents with polyuria, polydipsia, weight loss; DKA is a frequent initial emergency.
  • Diagnosis: RBS ≥200 mg/dL (symptomatic), FBS ≥126 mg/dL, or HbA1c ≥6.5%.
  • DKA management: Prioritize IV fluids, insulin infusion, careful potassium replacement.
  • Honeymoon period: Temporary remission after initiating insulin therapy.
  • Long-term: Lifelong insulin, glucose monitoring, HbA1c target <7.0-7.5%, screen for complications.
  • MODY: Monogenic, autosomal dominant, non-ketotic familial hyperglycemia.

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