Type 1 Diabetes mellitus

Question 1

What actually is Diabetes Mellitus? (1)

Answer 1

• Inappropriate glucose homeostasis(Chronic hyperglycaemia)
• Most common endocrine disorder

Question 2

Describe diabetes mellitus and what the two types are?

Answer 2

• Chronic metabolic disorder charachterised by hyperglycaemia
• Two most common typesof DM:
  1. Insulin deficiency (Type 1) 5-15%
  2. Impaired B-cell function and/or loss of insulin sensitivity (insulin resistance) (Type 2) 85-95%

Question 3

What are the direct consequences of High blood glucose levels?

Answer 3

• Glucosaria, polyuria (due to osmotic diuresis), polydesia(thirst)
• Visual disturbance (altered refractive index of lens)
• ^Urimogenital infections

Question 4

What are the Metabolic consequences of impaired glucose utilization?

Answer 4

• Lethargy, weakness
• Weight loss
• Ketoacidosis

Question 5

What are the long-term complications of diabetes?

Answer 5

• Microvascular: Nephropathy, neuropathy, retinopathy
• Macrovascular: Ischaemic HD, Stroke, Peripheral vascular disease

Question 6

What are the aims of management of T1&2 DM?

Answer 6

• Alleviate symptoms
• Minimise the risk of long-term, secondary complications
  1. Microvascular
  2. Macrovascular

Question 7

What should T1&2 DM patients do with their diets?

Answer 7

• Healthy diet
• Regular meals-no skipping
• Low fat/sugar/salt
• High in fibre/complex carbs
• Lots of fruit&Veg
• Reg excercise-imp insulin sensitivity
• Red cardiovascular risk

Question 8

What is Type 1 Diabetes?

Answer 8

• Autoimmune
• Progressive destruction of islet B-cells
• Onset usually < 40years
• Rapid onset
• Treatment with insulin, regular excercise and healthy diet

Question 9

How is insulin released?

Answer 9

1. Incretins and parasympathetic NS Inc release
2. Sympathetic NS dec release

• Preproinsulin–>Proinsulin–>Insulin

Question 10

What is the role of insulin?

Answer 10

• Acts on insulin receptor
• Tyrosine Kinase receptor
• Stimulates glucose into skeletal muscle through inc in GLUT-4 transporters
• Stimulates conversion of glucose into glycogen in liver
• Prevents glycogen breakdown
• Inhibits synthesis of glucose (gluconeogenesis)
• stimulates lipogenesis- storage of fat
• Inhibits food intake
• Stimulates cells to take up Potassium

Question 11

How are insulin therapies classified?

Answer 11

1. Short acting
2. Intermediate
3. Long acting

Question 12

What are short acting insulin therapies?

Answer 12

• Human insulin analogues
  1. Soluable
  2. Rapid acting
• Normally insulin forms into hexamers which break into monomers to be absorbed into blood stream
• Recombinant analogues are modified to remain as monomers-Inc rate of absorption

Question 13

What are Intermediate and Long acting insulin therapies?

Answer 13

• Mix of insulin complexed with other ingredients
• Gradually absorbed into blood stream
• E.g. Insulin Isophane (complexed with protoamine NPH)—Intermediate acting
• Insulin glargine and insulin detemir-long acting (24 hours)

(see PP for action profiles)

Question 14

What is Detemir-14?

Answer 14

• Carbon fatty acid (Myristic acid) bound which promotes binding to albumin
• Dissociates slowly from albumin
• Insulin glargine–structural changes to insulin molecule make it less soluable at physiological pH
• Precipitates on injection–Leads to slow absorption from subcutaneous Space

Question 15

What is an insulin pump?

Answer 15

• Continuous subcutaneous insulin infusion (CSII)
• Regular monitoring is essential for good glycaeimc control
• —–Minimise acute and long-term (secondary) complications of DM