Diabetes Mellitus By Harvi & Manpreet

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

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

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

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

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

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

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

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

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