1. Diabetes Mellitus By Harvi & Manpreet

2. What Is It?  complex metabolic disorder  elevated blood glucose concentration  secondary to resistance to action of insulin or insufficient insulin or both  concerns beta cells of islets of langerhans

3. Type 1 VS Type 2 Type 1Type 2 Onsetearlylater life Triggersinfections or idiopathic high BMI & hyperglycaemia Ketoacidosis (DKA)more likely if poorly controlled rare Treatmentinsulin or pancreatic transplants (rare) attempt lifestyle interventions before pharmacological interventions Prognosisno recovery to beta cells weight loss and exercise

4. DM Symptoms  polyuria  polydipsia  weight loss  nocturia  fatigue  slow wound healing  repeated UTIs  blurred vision

5. Steps Of Insulin Secretion 1. extracellular glucose is transported into the beta cell via GLUT 2 2. glucose is metabolised which increases ATP:ADP ratio within the cell 3. this causes the closure of ATP-dependent potassium channels 4. closure of potassium channels leads to cell membrane depolarisation 5. membrane depolarisation causes opening of voltage-gated calcium channels and an influx of calcium into the cell 6. calcium influx leads to exocytosis of stored insulin vesicles

6. Complications Of DM Microvascular  nephropathy  retinopathy  neuropathy Macrovascular  ischaemic heart disease  cerebrovascular disease  peripheral vascular disease

7. Diabetic Ketoacidosis (DKA)  medical emergency  characterising hallmarks = hyperglycaemia, acidosis and high ketones  can be triggered by precipitating conditions or physiological stresses

8. Signs Of DKA Early  worsening polydipsia  worsening polyuria Acute/Late  decreased consciousness  hypotension  tachycardia  hyperventilation  abdominal discomfort

9. Treatment Of DKA  Insulin IV  Rehydration Therapy: IV Fluids  Possibly Bicarbonate Replacement

10. Thanks For Listening!