Type 1 diabetes Flashcards

1
Q

Define T1D.

A

· Metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency.

· Develops due to destruction of pancreatic beta cells.

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2
Q

What is the epidemiology of T1D?

A

· Accounts for 5-10% of all patients with diabetes.
· More common in Europeans.
· Less common in Asians.
· Commonly presents when young.

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3
Q

What is the pathophysiology of T1D?

A

· Autoimmune pancreatic beta cell destruction in genetically susceptible individuals.
· Beta cell destruction proceeds sub-clinically for months to years as insulitis (beta cell inflammation).
· When 80-90% of beta cells are destroyed, hyperglycaemia develops.
· Patients are unable to utilise glucose in peripheral muscle and adipose tissues.
· This stimulates the secretion of counter-regulatory hormones such as glucagon, adrenaline, cortisol and GH.
· These promote gluconeogenesis, glycogenolysis and ketogenesis in the liver.
· Patients then present with hyperglycaemia and anion gap metabolic acidosis.

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4
Q

Untreated T1D can lead to what fatal condition?

A

DKA.

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5
Q

What is the aetiology of T1D?

A

· Certain HLA gene polymorphisms increases susceptibility to or provide protection from the disease.
· In susceptible people, environmental factors may trigger the immune-mediated destruction of beta cells.
· Coeliac disease shares a HLA genotype with type 1 diabetes, and is more common in those with type 1.

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6
Q

List the possible risk factors of T1D.

A

· Geographic location.
· Genetic predisposition.
· Young age.

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7
Q

What are the typical presenting signs and symptoms?

A
· Polyuria. 
· Polydipsia. 
· Weight loss. 
· Blurred vision. 
· N&V, abdominal pain, tachypnoea, lethargy and coma - suggests DKA.
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8
Q

What investigations would you request if you suspected a patient had T1D?

A

· Random plasma glucose >11mmol/L.
· Fasting plasma glucose >6.9.
· 2-hour plasma glucose - plasma glucose is measured 2 hours after 75g oral glucose load - >11.
· Plasma or urine ketones.
· HbA1C >48mmol/mol
· Fasting C-peptide - low or undetectable.

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9
Q

Differentials?

A

· Maturity onset diabetes of the young (MODY).

Type 2 diabetes.

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10
Q

What is the treatment regime for a non-pregnant T1D?

A

· 1st line - Basal-bolus insulin.
· Adjunct - Pre-meal insulin correction dose.
· Adjunct - Amylin analogue.
· 2nd line - Fixed-dose insulin: e.g. Isophane human/insulin neutral, injected subcutaneously.

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11
Q

What is the treatment regime for a pregnant T1D?

A

· 1st line - Basal-bolus insulin: injected subcutaneously– if pregnant give insulin isophane human (NPH).
· Plus - Low-dose aspirin.

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12
Q

What complications can arise?

A

DKA:
· Missed insulin injections or physiological stresses such as infection or a MI.
· Hyperglycaemia and ketosis cause osmotic diuresis leading to dehydration.

Hypoglycaemia.

Retinopathy.

Diabetic kidney disease.

Peripheral or autonomic neuropathy.

Cardiovascular disease.

Microvascular complications:
· Retinopathy.
· Nephropathy.
· Neuropathy.

Macrovascular complications:
· Coronary artery disease.
· Cerebrovascular disease.
· Peripheral vascular disease.

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