Makindo Medical Notes

Related Subjects: Type 1 DM |Type 2 DM |Diabetes in Pregnancy |HbA1c |Diabetic Ketoacidosis (DKA) Adults |Hyperglycaemic Hyperosmolar State (HHS) |Diabetic Nephropathy |Diabetic Retinopathy |Diabetic Neuropathy |Diabetic Amyotrophy |Maturity Onset Diabetes of the Young (MODY) |Diabetes: Complications

Type 1 diabetes results from autoimmune destruction of insulin-producing cells (ß cells) in the pancreas, leading to marked insulin deficiency and resultant hyperglycaemia. People with Type 1 diabetes require insulin therapy to prevent diabetic ketoacidosis.

Basic Blood Glucose Ranges (UK and US Units)

About

• Autoimmune destruction of beta cells results in insulin loss.
• Daily endogenous insulin production is typically 16-24 units.
• Insulin is essential for glucose and potassium entry into cells; deficiency leads to hyperglycaemia, ketosis, and diabetic ketoacidosis (DKA).
• Requires replacement with exogenous insulin.

Aetiology

• Autoimmune destruction of islet cells, often associated with HLA-D3 and HLA-D4.
• T-cell-mediated autoimmune attack on pancreatic beta cells.
• C-peptide can be assayed to assess endogenous insulin secretion.
• High glutamic acid decarboxylase (GAD) antibodies, especially useful in diagnosing latent autoimmune diabetes of the adult (LADA).

Clinical Presentation

• Polyuria, polydipsia, weight loss, blurred vision.
• Infections such as oral/genital candidiasis.
• Diabetic ketoacidosis: ketone breath, Kussmaul’s respiration.

Later Complications

• Ophthalmological: Cataract, retinopathy (proliferative and non-proliferative), macular oedema, rubeosis, glaucoma.
• Renal/Nephropathy: Proteinuria, end-stage renal failure, Type IV renal tubular acidosis.
• Neurological: Distal symmetrical polyneuropathy, autonomic neuropathy, diabetic amyotrophy.
• Gastrointestinal: Gastroparesis, fatty liver, diarrhoea, constipation.
• Genitourinary: Cystopathy, erectile dysfunction, vaginal candidiasis.
• Cardiovascular: Ischaemic heart disease, heart failure, peripheral vascular disease, stroke.
• Lower Limb Complications: Ulceration, Charcot joint, amputation risk.
• Dermatology: Cellulitis, furunculosis, necrobiosis, acanthosis nigricans.
• Dental: Periodontal disease, candida.
• Psychological: Depression, anxiety.

International Definitions

• Normal fasting sugar: < 6.1 mmol/L [110 mg/dL] and 2 hr < 7.8 mmol/L [140 mg/dL]
• Diabetes: Fasting blood sugar > 7.0 mmol/L [126 mg/dL]
• Impaired glucose tolerance: OGTT 2 hr glucose 7.8-11 mmol/L [140-199 mg/dL]
• Diabetes: Random blood glucose > 11.1 mmol/L [200 mg/dL] + symptoms

Investigations

• Islet cell antibodies (ICA): ~80% prevalence in Type 1.
• GAD antibodies: ~90% prevalence in Type 1.
• Insulin autoantibodies (IAA), FBC, U&E, lipid profile, ECG, retinal photography.

Management (All Patients Require Insulin)

• Weight loss, dietary advice, risk factor management, smoking cessation, exercise.
• Various insulin regimens aim to mimic normal physiological responses; normal requirements are 16-24 units/day.
• Initial period may see a temporary reduction in insulin needs ("honeymoon period").

Insulin Regimens

• Subcutaneous injections at different sites to avoid local complications.
• Mixed Intermediate/Soluble Insulin: Administered twice daily.
• Basal/Bolus Regimen: 50-60% as a long-acting basal dose with short-acting insulin at mealtimes.
• Insulin Pump: Consider for patients with HbA1c > 7.5% despite basal-bolus regimen.
• Acute Illness Management: Continue basal-bolus doses, increase insulin if poor glucose control. If unwell and unable to eat, may require IV fluids and potentially sliding scale insulin.