Diabetes Flashcards
Ideally the body wants to keep blood glucose at at a concentration between ?
4.4 and 6.1 mmol/L
Where is insulin produced ?
The beta cells in the Islets of Langerhans in the pancreas
What type of hormone is insulin ?
It is an anabolic hormone
How does insulin reduce blood sugar levels ?
-It causes cells in the body to absorb glucose from the blood and use it as fuel
-It causes muscle and liver cells to absorb glucose from the blood and store it as glycogen
Where is glucagon produced ?
The alpha cells in the Islets of Langerhans in the pancreas
What type of hormone is glucagon ?
It is a catabolic hormone
What is glucagon released in response to ?
Low blood sugar levels and stress
How does glucagon increase blood sugar levels ?
-Glycogenolysis
-Gluconeogenesis (It tells the liver to convert fats and proteins into glucose
When does ketogenesis occur ?
When there is insufficient glucose supply and glycogen stores are exhausted, such as in prolonged fasting
What happens in ketogenesis ?
The liver takes fatty acids and converts them into ketones. Ketones are water soluble fatty acids that can be used as fuel. The can cross the BBB and can be used by the brain. Producing ketones is normal and not harmful in healthy pts when under fasting conditions or on very low carbohydrate, high fat diets.
How can ketone levels be measured ?
-Urine dip stick
-In the blood using a ketone meter
People with ketosis have a characteristic what smell on their breath ?
Acetone smell
Ketone acids (ketones) are buffered in normal pts so the blood does not become acidotic. When underlying pathology (i.e. type 1 diabetes) causes extreme hyperglycaemic ketosis this results in what ?
A life threatening metabolic acidosis. This is called diabetic ketoacidosis.
Pathophysiology of DKA ?
DKA occurs in type 1 diabetes where the person is not producing adequate insulin themselves and is not injecting adequate insulin to compensate for this. It occurs when the body does not have enough insulin to use and process glucose. The main problems are ketoacidosis, dehydration and potassium imbalance.
KETOACIDOSIS:
-As the cells in the body have no fuel and think they are starving they initiate the process of ketogenesis so that they have a usable fuel. Over time the pt gets higher and higher glucose and ketone levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH. Over time the ketone acids use up the bicarbonate and the blood starts to become acidic. This is called ketoacidosis.
DEHYDRATION:
-Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes polyuria. This results in severe dehydration. The dehydration stimulates the thirst centre to tell the pt to drink lots of water causing polydipsia.
POTASSIUM IMBALANCE:
-Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in t the urine, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts pts can develop severe hypokalaemia very quickly and this can lead to fatal arrhythmias
Presentation of DKA ?
This is a life threatening medical emergency. The pathophysiology described previously leads to:
-Hyperglycaemia
-Dehydration
-Ketosis
-Metabolic acidosis (with a low bicarbonate)
-Potassium imbalance
The pt will therefore present with symptoms of these abnormalities:
-Polyuria
-Polydipsia
-Nausea and vomiting
-Acetone smell to their breath
-Dehydration and subsequent hypotension
-Altered consciousness
-They may have symptoms of an underlying trigger (i.e. sepsis)
Note:
The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis. Therefore the priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones.
Diagnosis of DKA ?
Check the local DKA diagnostic criteria for your hospital. To diagnose DKA you require:
-Hyperglycaemia (i.e. blood glucose > 11 mmol/L)
-Ketosis (i.e. blood ketones > 3 mmol/L)
-Acidosis (i.e. pH < 7.3)
Treatment of DKA ?
FIG-PICK
Follow local protocols carefully
F - Fluids - IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I - Insulin - Add an insulin infusion (e.g. Actrapid at 0.1 Unit/Kg/hour)
G - Glucose - Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. < 14 mmol/L)
P - Potassium - Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I - Infection - Treat underlying triggers such as infection
C - Chart fluid balance
K - Ketones - Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)
Establish the pt on their normal subcutaneous insulin regime prior to stopping the insulin and fluid infusion.
Remember as a general rule potassium should not be infused at a rate of more than 10 mmol per hour.
Long term management of type 1 diabetes ?
Patient education is essential. Monitoring and treatment is relatively complex. The condition is life-long and requires the pt to fully understand and engage with their condition. It involves the following components:
-Subcutaneous insulin regimes
-Monitoring daily carbohydrate intake
-Monitoring blood glucose on waking, at each meal and before bed
-Monitoring for and managing complications, both short term and long term
Insulin is usually prescribed as a combination of a background, long acting insulin given once a day and a short acting insulin injected 30 minutes before intake of carbohydrates (i.e. at meals). Insulin regimes are initiated by a diabetes specialist.
Injecting into the same spot can cause a condition called “lipodystrophy”, where the subcutaneous fat hardens and pts do not absorb insulin properly from further injections in this spot. For this reason pts should cycle the injection sites. If a pt is not responding to insulin as expected, ask where they inject and check for lipodystrophy.
Short term complications of type 1 diabetes ?
-Hypoglycaemia
-Hyperglycaemia (and DKA)
