Weight loss in a person with normal BMI (<25)
Polyuria, polydipsia, and nocturia
Sudden onset of sx
Ketosis or ketonuria
Age <50 years
Personal or family history of autoimmune diseases (e.g., coeliac disease, autoimmune thyroiditis)

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Investigations

Blood glucose levels (random ≥11.1 mmol/L or fasting ≥7.0 mmol/L)
Ketones:
- Blood ketones >0.5 mmol/L indicate ketosis; >1.5 mmol/L is an emergency
- Urine ketones (used if blood ketone testing is unavailable)
Autoimmune markers:
- Glutamic acid decarboxylase (GAD) antibodies
- Insulinoma antigen-2 (IA-2) antibodies
- Zinc transporter-8 (ZnT8) antibodies (if avail)
C-peptide (low in T1DM, helps differentiate from T2DM and latent autoimmune diabetes in adults)

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Notes:

Islet-cell antibodies are no longer routinely used; IA-2 antibodies are preferred
A blood ketone level >1.5 mmol/L suggests DKA, requiring urgent specialist input.

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T1DM in Adults vs Children/Adolescents

Honeymoon Phase
- Adults: Often over 12 months.
- Children: Typically lasts 6–12 months.
Glycaemic Targets
- Adults: HbA1c ≤ 7% (53 mmol/mol), fasting glucose 4–7 mmol/L, postprandial glucose 6–10 mmol/L.
- Children/Adolescents: HbA1c ≤ 7% (same target), but higher caution required in young children to avoid severe hypoglycaemia during rapid brain growth.
Complication Screening
- Adults: Annual screening for microvascular (e.g., retinopathy, nephropathy) and macrovascular complications (e.g., cardiovascular disease).
- Children/Adolescents: Chronic complications (e.g., retinopathy, kidney disease) are rare in childhood; routine screening begins after 5 years of disease onset or age 11.
Dietary Management
- Adults: Focus on glycaemic control and weight management.
- Children: Nutritional intake tailored to growth, energy needs, and puberty; education for family members is critical.

T1DM

Classic Symptoms:

Polyuria and Polydipsia: Frequent urination and excessive thirst due to osmotic diuresis from hyperglycemia.
Polyphagia: Increased hunger resulting from energy depletion in tissues.
Weight Loss: Typically occurs despite normal or increased food intake, especially in individuals with a normal BMI (<25).
Ketosis/Ketonuria: Presence of ketone bodies in urine or blood due to lipolysis when insulin is deficient.

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Onset of Symptoms:

Sudden Onset: Rapid development of symptoms is common, unlike in Type 2 diabetes.
Often presents in individuals aged <50 years, though it can develop at any age.

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Family and Personal History:

Autoimmune Diseases: Ask about a personal or family history of autoimmune conditions, as T1DM is associated with other autoimmune disorders (e.g., thyroid disease, coeliac disease).

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Pathophysiology

Mechanism: Autoimmune destruction of beta cells leads to absolute insulin deficiency, causing hyperglycaemia and associated metabolic disturbances.
Stages in Development:
- Genetic predisposition, followed by autoimmune activation and eventual beta-cell destruction.

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Investigations

Blood Glucose Testing:

Random Blood Glucose: Elevated levels (>11.1 mmol/L) with classic symptoms can confirm the diagnosis.
Fasting Blood Glucose: Elevated levels (>7 mmol/L) support the diagnosis.

Blood Glucose with Ketones:

Blood Ketones: Suspect T1DM if blood glucose is elevated with blood ketones >0.5 mmol/L (levels >1.5 mmol/L indicate a high risk for DKA and are an emergency).

Autoantibodies:

Glutamic Acid Decarboxylase (GAD) Antibodies: Commonly present in T1DM and used to differentiate from Type 2 diabetes.
Insulinoma Antigen-2 (IA-2) Antibodies: Another marker for T1DM.
Other Autoantibodies: Occasionally, zinc transporter 8 (ZnT8) antibodies may also be tested.

C-Peptide:

Low C-Peptide: Indicates low endogenous insulin production, which is characteristic of T1DM. Helps differentiate from Type 2 diabetes, where C-peptide levels are usually normal or elevated.
- <0.2 nmol/L in fasting or non-fasting state suggests T1DM.

Note:

Islet-Cell Antibodies: Previously used but now IA-2 antibodies are preferred for diagnosis.

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Management

Insulin Therapy:

Basal-Bolus Regimen: Combination of long-acting basal insulin (e.g., glargine or detemir) and short-acting bolus insulin (e.g., aspart or lispro) before meals.
Continuous Subcutaneous Insulin Infusion (CSII): Insulin pumps may be considered in patients with difficulty achieving control on injections.

Monitoring:

Self-Monitoring of Blood Glucose (SMBG): Regular checks to adjust insulin doses and prevent hypoglycemia.
Continuous Glucose Monitoring (CGM): Can provide real-time glucose levels and trends to aid in glycemic control.

Education:

Carbohydrate Counting: Essential for adjusting insulin doses based on meal content.
Hypoglycemia Management: Education on recognising and treating low blood glucose episodes, including using glucagon in emergencies.

Preventive Care:

Screening for Complications: Regular checks for retinopathy, nephropathy, and neuropathy.
Vaccinations: Recommend vaccinations (e.g., influenza, pneumococcal) due to increased risk of infections.

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Complications

Diabetic Ketoacidosis (DKA):

A life-threatening emergency due to insulin deficiency, resulting in hyperglycemia, acidosis, and dehydration.
Management includes IV fluids, insulin infusion, electrolyte replacement, and monitoring.

Long-Term Complications:

Microvascular: Retinopathy, nephropathy, and neuropathy.
Macrovascular: Increased risk of cardiovascular disease.

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Special Considerations:

Adolescents and young adults may experience challenges with adherence and glycemic variability.
Screen for other autoimmune disorders, such as autoimmune thyroid disease and coeliac disease, at diagnosis and periodically thereafter

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