Diabetes type 1 Flashcards
Define
- Metabolic hyperglycaemic condition caused by absolute insufficiency of pancreatic insulin production
- Autoimmune or idiopathic (absence of antibodies, strong genetic component)
- Latent autoimmune diabetes of adults (slower progression)
What’s the aetiology?
• Caused by destruction of pancreatic insulin-producing beta cells
• Autoimmune process
• Concordance is only about 30% in identical twins, indicating environmental influence
• Occurs in genetically susceptible individuals with an environmental trigger
• Associated with other autoimmune diseases
• Autoantigens associated with T1DM:
o Glutamic acid decarboxylase (GAD)
o Insulin
o Insulinoma-associated protein 2
o Cation efflux zinc transporter
What’s the pathophysiology?
Beta-cell destruction proceeds sub-clinically for months to years as insulitis (inflammation of the beta cell). When 80% to 90% of beta cells have been destroyed, hyperglycaemia develops. Insulin resistance has no role in the pathophysiology of type 1 diabetes. However, with increasing prevalence of obesity, some patients with type 1 diabetes may be insulin resistant in addition to being insulin deficient.
Patients with insulin deficiency are unable to utilise glucose in peripheral muscle and adipose tissues. This stimulates the secretion of counter-regulatory hormones such as glucagon, adrenaline (epinephrine), cortisol, and growth hormone. These counter-regulatory hormones, especially glucagon, promote gluconeogenesis, glycogenolysis, and ketogenesis in the liver. As a result, patients present with hyperglycaemia and anion gap metabolic acidosis.
What are the symptoms?
- Juvenile onset (< 30 yrs) – typically 5 to 15
- Polyuria/nocturia
- Polydipsia
- Tiredness
- Weight loss
- Blurred vision
What are the signs?
• Signs of complications:
o Fundoscopy - check for diabetic retinopathy
o Examine feet for evidence of neuropathy (monofilament test, pulses)
o Monitor BP
• Signs of associated autoimmune conditions
o Vitiligo
o Addison’s disease
o Autoimmune thyroid disease
What are the appropriate investigations?
- Blood Glucose - fasting blood glucose > 7 mmol/L or random blood glucose > 11.1 mmol/L
- 2 hour plasma glucose – plasma glucose measured 2 hours after 75g oral glucose load, >11.1mmol/l
- HbA1c – reflects degree of hyperglycaemia over 3 months, >48mmol/mol
- Urine - glycosuria, ketonuria, MSU
- FBC - MCV, reticulocytes
- U&Es - monitor for nephropathy and hyperkalaemia
- Lipid profile
- Urine albumin creatinine ratio - used to detect microalbuminuria
- Autoimmune markers – autoantibodies mentioned above
What;s the management plan?
• Glycaemic Control
o Advice and patient education
• Short-acting insulin (three times daily before meals):
Lispro
Aspart
Glulisine
• Long-acting insulin (once daily):
Isophane
Glargine
Detemir
o Insulin pumps
o DAFNE courses (dose adjustment for normal eating)
o Monitor
• Regular capillary blood glucose tests
• HbA1c every 3-6 months
o Screening and management of complications
o Treatment of hypoglycaemia
• If reduced consciousness: 50 ml of 50% glucose IV OR 1 mg glucagon IM
• If conscious and cooperative: 50 g oral glucose + starchy snack
o Screening and management of cardiovascular risk factors
What are the possible complications?
• Diabetic ketoacidosis o Can be precipitated by infection, errors in management of diabetes, newly diagnosed diabetes, idiopathic • Microvascular complications: o Retinopathy o Nephropathy o Neuropathy • Macrovascular complications: o Peripheral vascular disease o Ischaemic heart disease o Stroke/TIA • Increased risk of infection • Complications of treatment: o Weight gain o Fat hypertrophy at insulin injection sites o Hypoglycaemia • Personality changes • Fits • Confusion • Coma • Pallor • Sweating • Tremor • Tachycardia • Palpitations • Dizziness • Hunger • Focal neurological symptoms
What’s the prognosis?
- Depends on early diagnosis, good glycaemic control and compliance with treatment and screening
- Vascular disease and renal failure are the main causes of increased morbidity and mortality
