1. Diabetes

2. Islet of Langerhans

3. Insulin Secretion Glucose enters β cell via GLUT2. Increase ATP concentration ATP-sensitive K + channel inactivated. Increased K + in cell gives depolarisation This opens a voltage-gated Ca 2+ channel Calcium influx causes insulin-containing vesicles to bind with membrane and exocytose. (Releases insulin)

5. Type I vs. II DM Type IType II Usually early onsetLater life onset Autoimmune destruction of β- cells Insulin resistance and exhaustion of β-cells Can be triggered by infections or can be idiopathic High BMI and hyperglycaemia trigger diabetes Can get ketoacidosis if not controlled Very rare for ketoacidosis Treatment is insulin or pancreatic transplants (rare) Attempt lifestyle interventions before moving on to drugs No recovery of cellsWeight loss and exercise can result in great improvements in condition 5-10% of diabetes90-95% of diabetes

6. Ketoacidosis Glucagon -> Glucose (glycogenolysis) Proteins -> Glucose (gluconeogenesis) Fat -> Ketones (lipolysis) Type I Diabetes and Hyperglycaemia. Fast, deep breathing to compensate Hyperglycaemia means glucose enters urine, taking water with it. Fall in pH, ketoacidosis Coma Death Compensation in lungs Kidney Dehydration Pear drop breath

7. Diabetes Symptoms Weight loss Polyuria, polydipsia, nocturia Tiredness Slower healing of wounds Repeated UTIs/thrush Blurring of vision.