Glycemic Emergencies Flashcards
Hypoglycaemia definition and causes
- BGL <4mmol/L or <2.5mmol/L (neonates)
- Depetion of glucose due to lack overdose of insulin from infection, starvation, exercise induced consumption or excessive alcohol (inhbits gluconeogensis)
Hypoglycaemia signs & symptoms
- Diaphoretic, pale and cool due to adrenaline release
- Altered GCS
- Hunger
- Anxiety
- Tachycardia
- Headache, confusion, drowsniess
- Clurred speech
- Siezures, unconsciousness, coms
Management of hypoglycaemia for alert patient
BGL <4mmol/L:
1. PO glucose paste 15g
2. Inadequate response: glucagon IM 1mg (adult and >25kg) or 0.5mg glucagon (<25kg)
3. IV glucose 10% (15g in 150mL) or 5ml/kg paed (stat dose only)
3. Low GI CHO
Management of hypoglycaemia for not alert patient
- IV access - IV glucose 10% (15g in 150mL) or (5ml/kg - paed), repeated every 5 mins until BGL >4mmol/L (one dose only for paed)
2 No IV access: IM glucagon 1mg - Follow up with low GI CHO
Neonate hypoglycaemia management
- BGL <2.5mmol/L
- PO glcuose gel 0.5ml/kg dose using a 3ml syringe, gently massage buccal area with gloved hand
Insulin effects
- Produced by beta cells in the pancreas
- Stimulate uptake of glucose from blood into cells
- Release is stilulated by an increase in BGL
- Promotes glycogensis in the liver and skeletal muscle
- Inhibits gluconeogensis and prevents glycogenolysis and lipolysis
Glucagon effects
- Produced by alpha cells in the pancreas
- Travels to liver via portal vein where is stimulates glycogenolysis in the liver.
- Maintains BGL inbetween meals and fasting
- Stimulates gluconeogensis and lipolysis
- Inhibited by high BGL
Adrenal cortex role in glycaemic management
- During periods of hypoglycaemia, adrenal medulla releases catecholamines such as adrenaline and NAD which stilulates glycogenolysis and lipolysis
- Also releases growth hormone and cortisol in response to proglonged hypoglycaemia to stimulate gluconeogenesis
T1DM definition & pathophysiology
- Autoimmune resonse where the body destroys beta cells, resulting in cessation of insulin production.
- Characterised by high BGL, weightloss, polyuria, polydipsia and polyphagia.
- Despite high BGL, cells are depleted of glucose > cellular starvation leads to gluconeogensis via the liver and lipolysis > increase in ketones due to lipolysis leads to ketoacidosis > metabolic acidosis leads to glucose in urine and dehydration.
T2DM pathophysiology
- Lifestyle related and develops later in life due to desensitisation of glucose receptors on cell surface.
- More insulin is secreted to maintain normal BGL inthe presence of excess glcuose but overtime beta cells become exhausted and secretion declines.
DKA pathophysiology
- Osmotic diuresis causes polyuria and polydipsia as excess glcuose moves through the glumerular capsule, into nephron, resulting in hyperosmolarity, pulling water into the distal convuluted tubule, leading to polyuria.
- Cellular dehydration due to increased osmotic pressure in ECF as a result og high BGL, leads to thirst.
- Weight loss as lipolysis occurs
- Electrolyte disturbances: ketoacidosis leads to vomiting, increasing dehydration and loss of electrolytes.
DKA signs & symptoms
Characterised by:
- Ketoacidosis
- Metabolic acidosis
- BGL >12mmol/L
Other:
- hot, flushed skin
- Confusion, agitiation
-n/v
- dehydration, increased thirst and hunger
- Tachycardia
- weakness
- polyuria, polydpsia
- coma
HHS pathophysiology
- Results from a lack of insulin causes an increase in circulating BGL
- Don’t produce ketones because small amount of glucos eis uptaken into cells, inhibiting production of ketaones.
- Pts presents significantly hyperglycaemia (generaly occurs over a longer period of time).
HHS Signs & Symptoms
- Significant hyperglycaemia (>30mmol/L)
- Hyperosmolarity due to increased glucose in ECF and dehydration
- Severe dehydration
Euglycaemic Ketoacidosis
Normal BGL, raise ketones
- More common in pregnanacy, low CHO diet and SGLT2 inhibits.
