diabetes

• diabetes

  fasting plasma glucose over 7mmol/L or 2h post prandial glucose over 11mmol/L
• type 1 diabetes

  insulin dependant, juvenile onset, autoimmune response, symptoms appear after 70% of beta cells are destroyed, high occurrence of hypoglycaemia and ketoacidosis
• type 1 genetic component

  influence susceptibility and resistance but doesn't follow a simple pattern of inheritance, HLA complex with DR and DQ alleles are thought to be involved and play a part in the immune system
• type 1 environmental cause

  enterovirus most likely, nutrition, hygiene, risk increases as you move further from the equator
• enterovirus

  induction of autoantibodies, induction of B cell lysis
• type 1 clinical presentations

  polyuria, polydipsia, polyphagia, loss of weight, high blood glucose levels, high glucose concentrations in urine, high levels of acetone in breath and urine
• polyuria

  passing large volumes of urine, leading to dehydration
• polydipsia

  excessive thirst
• polyphagia

  increased hunger
• glucosuria

  high glucose concentrations in urine
• ketoacidosis

  high levels of acetone in breath and urine
• hyperglyceaemia

  high plasma glucose concentrations, decreased or no insulin production, symptoms due to beta cell destruction
• hyperglycaemia results in:

  glucose remaining in plasma, increased glycogenolysis and gluconeogenesis, and blood gluocse to rise to over 10mmol/L
• during hyperglycaemia, the amount of glucose filtered by the kidney exceeds its capacity to reabsorb glucose, and it remains in filtrate to be excreted in urine (glucosuria)
• Normally, as glucose comes through, transporters reabsorb glucose, meaning there will be no glucose in the urine
• glucose has an osmotic effect which prevents the reabsorption of water back into the body from the kidney filtrate, more is lost in the urine (osmotic diuresis)
• No insulin leads to limited glucose uptake in insulin sensitive tissues and no suppression of glucagon secretion, glucagon stimulates HSL to increase lipolysis and gluconeogenesis. overtime, this leads to weight loss and excessive hunger and the body acts as it would during starvation
• ketoacidosis

  Accumulation of acetyl CoA in the liver due to increased lipolysis and gluconeogenesis, resulting in the production of ketone bodies
• A build-up of ketone bodies will lead to sweat fruity smelling breath (acetone) and ketoacidosis
• ketoacidosis leads to

  decreased serum pH, increased lung ventilation, depression of CNS (lethargy, confusion, decreased responsiveness)
• Sequence of events in type 1 diabetes:

  insulin deficient, hyperglycaemia, glucosuria, polyuria, dehydration, polydipsia, polyphagia, ketoacidosis
• populations at risk for type 2 diabetes

  ATSI, pacific islanders, people over 45 with obesity and hypertension, women with polycystic ovary syndrome
• Insulin signalling cascade changes can lead to insulin resistance
• type 2 diabetes progression

  insulin resistance, impaired fasting glucose and impaired glucose tolerance, type 2 diabetes
• symptoms of type 2 diabetes

  blurred vision, fatigue, frequent or slow healing wounds

  Polyuria, polydipsia, polyphagia (not as severe as type 1)
• Fasting state

  normal is under 6.1mmol/l, and diabetes is above 7
• Random state

  normal is under 7.8 and diabetes is higher than 11mmol
• Oral glucose tolerance test

  normal is under 7.8mmol/l after 2 hours, impaired is between 7.8 and 11, and diabetes is over 11mmol/L
• gestational diabetes

  Insulin resistance usually develops due to the increased levels of growth hormone and placental hormones