Diabetic Emergencies Flashcards
Describe the Diabetic Emergency of Hypoglycaemia.
Include- What it is, insulin status, patient demographics, what causes it in diabetics & non diabetics
HYPOGLYCAEMIA:
What is it?- Low level of glucose in the blood
Insulin Status- Insulin excess (too much insulin)
Patient Demographics- Common in T1, or T2 who are insulin dependant
Causes- Diabetics: too much insulin and insufficient intake, Non-Diabetics: reduced intake, exercise,
Describe the Pathophysiology of Hypoglycaemia (in diabetic patients)
- Insulin is administered
- The level of insulin is not balanced out with an adequate amount of food (or there is too much excercise)
- Glucose uptake is increased (the insulin is moving all the glucose available INTO cells and out of the blood)
- Blood glucose levels drop
Describe the signs & symptoms of Hypoglycaemia
Key Signs & Symptoms: Low BGL (<4mmol), Reduced level of consciousness, Confusion, Tremors, Diaphoresis, Dizziness
What is the pre-hospital management of HYPOGLYCAEMIA?
[therapeutic & pharmacological]
Pre-hospital Management of Hypoglycaemia:
- If GCS is reduced- maintain airway (lateral/recovery position, head tilt chin life)
- Cannulate (aim for a small cannula in a large vein- as extravasation during glucose infusion can cause tissue necrosis)
- Do a head to toe assessment and see if they have an insulin pump. Turn it off, or remove the injection site as it may still be administering insulin
PHARMACOLOGY:
a) If alert + can swallow= glucose paste
b) If reduced GCS= Glucose 10% IV (15g/150mL)
c) If unable to cannulate= Glucagon IM (1g)
Describe the Diabetic Emergency of Diabetic Ketoacidosis
Include- What it is, insulin status, patient demographics
What DKA is- High glucose levels in the blood, and no insulin available to get it into cells results in the breakdown of fats and production of ketones
Insulin status- Absolute insulin deficiency
Patient Demographics- Most commonly occurs in Type 1 Diabetics, but in rare circumstances it can occur in Type 2 Diabetics
Describe the Pathophysiology of Diabetic Ketoacidosis
PATHOPHYSIOLOGY OF DKA:
- Insufficient insulin
- No glycolysis (glucose cant get into cells)
- Cells scream out for glucose
- Increased secretion of counter regulatory hormones (glucagon, cortisol, growth hormone, catecholamines- adreanline)
- Glucagon increases glycogenesis (glycogen to glucose)
- Cortisol increases catabolism (muscle to amino acids) and gluconeogenesis (amino acids to glucose)
- Cortisol + GH + Adrenaline increase Lipolysis (Tricylcerides into glycerol & fatty acids)
- Gluconeogenesis turns glycerol into glucose
- Ketogenesis turns fatty acids into Ketones
Describe the signs & symptoms of Diabetic Ketoacidosis
Key Signs & Symptoms:
Hyperglycaemia (as all glycogen, fats & proteins have been turned into glucose & theres no insulin to get it into the cells)
Polyuria (excessive urination) & polydipsia (excessive thirst)- as renal threshold is reached so osmotic diuresis means glucose (& fluid) is being excreted in urine
Dehydration [low BP, tachy, poor skin tugor] secondary to Polyuria
Kussmaul respiration/tachyponea (compensatory respiratory alkalosis- try to offset acidosis)
Acetone/fruity breath (as one of the ketones created is acetoacetic acid)
Nausea & vomiting (hyperglycaemic impaired gastro motility)
Dysrhythmias (hyperkalaemia, then hypokalaemia)
Describe the Diabetic Emergency of Alcoholic Ketoacidosis
Include- What it is, insulin status, patient demographics
ALCOHOLIC KETOACIDOSIS
What it is- High glucose levels and reduced availability of insulin results in the breakdown of fats and production of ketones as a result of a sudden increase in alcohol consumption and reduction in intake
Insulin Status- Chronic alcoholism increases insulin resistance (the decreases in insulin sensitivity)
Patient demographics- Occurs in patients with chronic alcoholism
Describe the Pathophysiology of Alcoholic Ketoacidosis
- Alcoholic has sudden increase in baseline Alcohol consumption (binge) + Decreased Oral intake = Low BGL
- Counter regulatory hormones are released
- Glucagon stimulates hepatic glycogenolysis (glycogen to glucose) BUT theres not enough stores of glycogen as liver is too damaged from yrs of alcoholism to store enough glycogen
- Gluconeogenesis is stimulated to make glucose out of amino acids BUT the enzymes needed for this are currently being used to break down the alcohol
- Body is desperate for glucose so turns to lipolysis (triglycerides to glycerol & fatty acids)
- Fatty acids broken down into ketones via ketogenesis
- Results in metabolic acidosis & buffering systems being utilised (resp alkalosis, removal of hydrogen ions- releases potassium)
What is the key difference in symptoms for patients with Alcoholic Ketoacidosis & Diabetic Ketoacidosis?
Alcoholic ketoacidosis:
= normal or low BGL
= severe dehydration (but due to alcoholism, not osmotic diuresis)
= no polyuria (renal threshold is never reached so no osmotic diuresis)
= much more severe abdo pain, nausea, vomiting
Describe the Diabetic Emergency of Hyperosmolar Hyperglycaemic Syndrome (HHS)
Include- What it is, insulin status, patient demographics
What it is- High glucose levels for a long period of time resulting in severe dehydration
Insulin status- Relative insulin deficiency (insulin levels are just high enough to prevent breakdown of fat stores- ketoacidosis- so no ketones produced)
Patient demographics- Only occurs in those with type 2 diabetes. Risk increases if pt has infection or use of steroids (counter regulatory hormones)
Describe the Pathophysiology of Hyperosmolar Hyperglycaemic Syndrome
- Insulin deficiency &/or counter regulatory hormone
- decreased glucose utilisation
- Need to increase glucose
3a. Increased Gluconeogenesis
3b. Increased Gluconeogenesis - Results in Hyperglycaemia
- Increased Osmotic diuresis/ glycosuria
- Increased Dehydration
- Increased Hyperosmolarity
Describe the signs & symptoms of Hyperosmolar Hyperglycaemic Syndrome and the pre-hospital treatment for it
Key Signs & Symptoms: High BGL (30+), Profound Dehydration (High HR, Low BP), Fatigue, Polyuria & Polydipsia, Nausea, vomiting, abdo pain
Treatment: Fluids
What is the Somogyi Effect?
[include brief statement of what it is + the pathophysiology of it]
SOMOGYI EFFECT= Early morning hyperglycaemia in insulin dependant diabetics
Pathophysiology-
- Too much insulin administered before bed/not balanced with adequate food intake.
- BGL drops really low
- Counter regulatory hormones released, glycogenolysis (glycogen to glucose) and gluconeogenesis (fats/proteins to glucose) occurs
- = HYPERGLYCAEMIA upon wakening
What is the ‘Dawn Phenomenon’?
[include brief statement of what it is + the pathophysiology of it]
Dawn Phenomenon= is a natural occurence in everyone & is why people may wake up with slightly elevated BGL.
Pathophysiology:
During the night, cortisol & growth hormone are released.
This decreases glucose uptake in the muscles and therefore increases BGL.
Upon wakening, BGL may be slightly elevated, but the body balances this out and this goes unnoticed
