Type 1 Diabetes Mellitus Flashcards
1
Q
What is the definition of type 1 diabetes mellitus (T1DM)? [2]
A
a class of diabetes mellitus due to insulin deficiency / caused by autoimmune destruction of insulin-secreting pancreatic beta cells
2
Q
What is the epidemiology of T1DM? [4]
A
- typically manifests in childhood and has an adolescent onset
- patient is usually lean
- concordance is ~30% in identical twins, indicating environmental influence
- Latent autoimmune diabetes in adults (LADA) - slower progression to insulin dependence in later life
3
Q
What is the aetiology of T1DM? [3]
A
- autoimmune disease with autoantibodies forming against insulin and pancreatic islet beta cells
- idiopathic
- genetic susceptibility with HLA-DR3 +/- HLA-DR4
4
Q
What are the risk factors for T1DM? [3]
A
- family history - HLA-DR3 or HLA-DR4 in >90%
- associated with other autoimmune diseases - autoimmune thyroid, coeliac disease, Addison’s disease, pernicious anaemia
- environmental factors - dietary constituents, enteroviruses, vitamin D deficiency
5
Q
What is the pathophysiology of T1DM? [4]
A
- autoimmune destruction of the pancreatic insulin-secreting beta cells by autoantibodies
- this causes insulin deficiency as there is insufficient insulin production
- continued breakdown of liver glycogen leading to glycosuria and ketonuria
- when blood glucose increases and reaches 10mmol/L, the body can no longer absorb glucose, so polydipsia and polyuria in an attempt to remove excess glucose
6
Q
What causes diabetic ketoacidosis? [4]
A
- results from a reduced supply of glucose and an increase in fatty acid oxidation
- increased production of acetyl-CoA leading to ketone body production
- that exceeds the ability of peripheral tissue to oxidise them, and lowers the pH of blood
- acidification of blood impairs the ability of haemoglobin to bind to oxygen
7
Q
What is the clinical presentation of T1DM? [5]
A
- patients with T1DM tend to be leaner
- polyuria and nocturia - no more glucose can be absorbed, so high levels of glucose excreted in urine, which draws in water too, so excess loss of water and glucose
- polydipsia - thirst due to loss of fluids and electrolytes
- weight loss - due to fluid depletion and accelerated breakdown of fat and muscle
- ketonuria - excess breakdown of fat and muscle, may progress to ketoacidosis if not treated
8
Q
How is T1DM diagnosed? [7]
A
symptomatic - 1 abnormal value
- symptoms of hyperglycaemia - polyuria, polydipsia, unexplained weight loss, visual blurring, lethargy
- fasting plasma glucose >7mmol/L OR
- random plasma glucose >11.1mmol/L
asymptomatic - 2 abnormal values
- fasting plasma glucose >7mmol/L AND/OR
- random plasma glucose >11.1mmol/L AND/OR
- oral glucose tolerance test (OGTT) - 2hr value >11.1mmol/L
haemoglobin A1c (HbA1c) 1. HbA1c >48mmol/mol (6.5%)
9
Q
What can cause secondary diabetes? [6]
A
- pancreatitis/pancreatectomy
- acromegaly
- Addison’s disease
- neoplasia of pancreas
- Cushing’s syndrome
- drugs - thiazides, beta-blockers
10
Q
What is the treatment for T1DM? [4]
A
- insulin is always indicated in T1DM
- synthetic insulin administered via subcutaneous injection
- vital to educate patients on how to self-adjust insulin doses
- modify diet and avoid binge drinking
11
Q
What are the two types of insulin? [2]
A
- short-acting insulin - given before meals and starts working within 30-60 mins
- long-acting insulin - used at bedtime and is slowly released from the injection site
12
Q
What are the complications of insulin treatment? [4]
A
- hypoglycaemia
- lipohypertrophy - at injection site
- insulin resistance
- weight gain