Flashcards in Diabetes Deck (52)
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 ?
-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 ?
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.
-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.
-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.
-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:
-Metabolic acidosis (with a low bicarbonate)
The pt will therefore present with symptoms of these abnormalities:
-Nausea and vomiting
-Acetone smell to their breath
-Dehydration and subsequent hypotension
-They may have symptoms of an underlying trigger (i.e. sepsis)
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 ?
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 ?
-Hyperglycaemia (and DKA)
Most pts are aware when they are hypoglycaemic by their symptoms however some pts can be unaware until severely hypoglycaemic. Typical sypmtoms are ? & More severe hypoglycaemia will lead to what ?
-Tremor, sweating, irritability, dizziness and pallor.
-Reduced consciousness, coma and death unless treated.
How is hypoglycaemia treated in type 1 diabetics (include treatment for severe hypoglycaemia ?
-A combination of rapid acting glucose such as lucozade and slower acting carbohydrates such as biscuits and toast for when the rapid acting glucose is used up.
-Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.
How is hyperglycaemia treated in type 1 diabetes ?
If the pt is hyperglycaemic but not in DKA then may require their insulin dose to be increased. Pts will get to know their own individual response to insulin and be able to administer a dose to correct the hyperglycaemia. Be conscious that it can take several hour to take effect and repeated doses could lead to hypoglycaemia. If they meet the criteria for DKA they need admission for treatment of DKA.
Long term complications of type 1 diabetes ?
Chronic exposure to hyperglycaemia causes damage to the endothelial cells of blood vessels. This leads to leaky, malfunctioning vessels that are unable to regenerate. High levels of sugar in the blood also causes suppression of the immune system, and provides an optimal environment for infectious organisms to thrive.
-Coronary artery disease is a major cause of death in diabetics
-Peripheral ischaemia causes poor healing, ulcers and "diabetic foot"
-Kidney disease, particularly glomerulosclerosis
Infection related complications
-Urinary tract infections
-Skin and soft tissue infections, particularly in the feet
-Fungal infections, particularly oral and vaginal candidiasis
Monitoring of type 1 diabetes ?
-Capillary blood glucose
-Flash glucose monitoring (e.g. FreeStyle Libre)
What is a HbA1c, how often is it measured/why is it measured in diabetic pts?
When we check HbA1c we are counting glycated haemoglobin, which is how much glucose is attached to the haemoglobin molecule. This is considered to reflect the average glucose level over the last 3 months because RBCs have a lifespan of around 3 to 4 months. We measure it every 3 to 6 months to track progression of the pts diabetes and how effective the interventions are. It requires a blood sample to be sent to the lab, usually a red top EDTA bottle.
How is capillary blood glucose measured ?
Using a little machine called a glucose meter that gives an immediate result. Pts with type 1 and type 2 diabetes rely on these machines for self monitoring their sugar levels.
Flash glucose monitoring (e.g. Freestyle libre) ?
This uses a sensor on the skin that measures the glucose level of interstitial fluid. There is a lag of 5 minutes behind blood glucose. This sensor records the glucose readings at short intervals so you get a really good impression of what the glucose levels are doing over time. This user needs to use a "reader" to swipe over the sensor and it is the reader that shows the blood sugar readings. Sensors need replacing every 2 weeks for the FreeStyle Libre system. It is quite expensive and NHS funding is only available in certain areas at present. The 5 minute delay also means it is necessary to do capillary blood glucose checks if hypoglycaemia is suspected.
Simplified pathophysiology of type 2 diabetes ?
Repeated exposure to glucose and insulin makes the cells in the body become resistant to the effects of insulin. It therefore requires more and more insulin to produce a response form the cells to get them to take up and use glucose. Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less. A continued onslaught of glucose on the body in light of insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia. Chronic hyperglycaemia leads to microvascular, macrovascular and infectious complications as previously described.