D&E - Diabetes Mellitus Flashcards
Pathophysiology of T1DM.
The pancreas stops being able to produce adequate insulin, meaning the cells of the body cannot absorb glucose from the blood.
This means the glucose levels in the blood continue to rise (ie. hyperglycaemia).
Aetiology of T1DM.
The underlying cause is not clear:
- ?inherited
- ?Coxsacki B and enterovirus trigger
Presentation of T1DM?
Triad of hyperglycaemia:
- polyuria
- polydipsia
- weight loss
Alternatively, patients may present with diabetic ketoacidosis.
Outline the metabolism of glucose and control of blood sugar.
As carbohydrates are digested, monosaccharides can be absorbed from the small intestine into the blood, causing a rise in blood glucose.
Beta cells in the Islets of Langerhans of the pancreas produce insulin, which acts to reduce blood glucose levels by:
- increasing glucose absorption by cells, where it is used as an energy source
- increasing glucose absorption by the liver, where it is stored as glycogen (glycogenesis)
As blood glucose levels fall, glucagon is produced by the alpha cells in the Islets of Langerhans of the pancreas, which acts to increase blood glucose levels by:
- increasing catabolism of glycogen into glucose (glycogenolysis)
- increasing anbolism of glucose from proteins and fats in the liver (gluconeogenesis)
The pancreas releases insulin and glucagon in response to fluctuations of blood glucose, aiming to maintain a concentration of 4.4 - 6.1 mmol/L.
Outline the role of ketones in the control of blood sugar.
When there is insufficient glucose supply and glycogen stores are exhausted, the liver converts fatty acids into ketones (ketogenesis) under the action of glucagon.
Ketones are water-soluble fatty acids, that can cross the blood-brain barrier and be used by the brain.
The kidney usually buffers ketone acids to prevent the blood becoming acidotic, however in insulin deficiency (T1DM) ketosis may be beyond the buffering capabilities of the kidneys…
What is the pathophysiology of diabetic ketoacidosis?
In T1DM, insulin deficiency reduces the body’s ability to perform glycogenesis and glucose transport into cells, where it is used for energy.
Under the influence of glucagon, the liver begins to produce ketones. Initially, the kidneys produce bicarbonate to buffer the ketone acids in the blood and maintain a normal pH.
In pronounced hyperketonaemia, the buffering capabilities of the kidneys are exhausted and the blood becomes acidic (ketoacidosis).
What are the common scenarios for diabetic ketoacidosis to occur?
- initial presentation of T1DM
- existing T1DM, unwell with infection
- existing T1DM, with poor treatment adherence
What are the key features of diabetic ketoacidosis?
- ketoacidosis
- dehydration
- potassium imbalance
Why does dehydration occur as a feature of diabetic ketoacidosis?
Hyperglycaemia and hyperketonaemia overwhelm the kidneys, and cause an increased oncotic pressure within the kidney tubules.
Osmotic diuresis increases water resorption by the kidneys, causing an increased urine production (polyuria).
Increasing water losses as urine results in dehydration. This causes the blood osmolality to increase, which stimulates the hypothalamus and results in excessive thirst (polydipsia).
Why does potassium imbalance occur as a feature of diabetic ketoacidosis?
Insulin usually drives potassium into cells.
In T1DM, insulin deficiency means potassium is not added to and stored in cells. This means that - while serum potassium may be eukalaemic - total body potassium is low as no potassium is stored in the cells.
When treatment with insulin starts, patients can develop severe hypokalaemia and subsequently fatal arrhythmias quickly.
Presentation of diabetic ketoacodisos.
- polyuria
- polydipsia
- dehydration
- acetone smell to breath
- weight loss
- n+v
- hypotension
- altered consciousness
Diabetic ketoacidosis may be triggered by an underlying condition, such as an infection. In any patient with DKA, it is also important to look for signs of infections and other underlying pathology that may need treatment.
How is diabetic ketoacidosis diagnosed?
- hyperglycaemia (>11mmol/L)
- ketosis (>3mmol/L)
- acidosis (<7.30)
How is diabetic ketoacidosis treated?
DKA is a medical emergency, which requires input from expert senior support.
FIG-PICK mnemonic:
- Fluids - IV fluid resuscitation with 0.9% NaCl
- Insulin - fixed rate insulin infusion
- Glucose - closely monitor blood glucose and add a glucose infusion when it is less than 14mmol/L
- Potassium - add potassium to IV fluids and monitor closely
- Infection - treat underlying triggers such as infection
- Chart fluid balance
- Ketones - monitor blood ketones, pH and bicarbonate
What are the key complications of DKA treatment?
- hypoglycaemia
- hypokalaemia
- cerebral oedema
- pulmonary oedema
Which autoantibodies are associated with T1DM?
- anti-islet cell antibodies
- anti-GAD antibodies
- anti-insulin antibodies
Serum C-peptide is a measure of insulin production.
How is T1DM managed in the long term?
- subcutaneous insulin
- monitoring dietary carbohydrate intake
- monitoring blood sugar levels upon waking, at each meal and before bed
- monitoring for and managing complications
What is a basal-bolus regime?
A combined insulin therapy regime:
- background, long-acting insulin injected once a day
- short-acting insulin injected 30 minutes before meals
What is a common side effect of insulin injections?
Injecting into the same spot can cause lipodystrophy, where the subcutaneous fat hardens. These areas do not absorb insulin properly from further injections.
Patients should cycle their injection sites to avoid lipodystrophy.
What are insulin pumps?
An alternative to basal-bolus insulin regimes, where insulin is continuously infused at different rates to control blood sugar levels.
They allow better blood sugar control, meaning patients have more flexibility with eating (and fewer injections).
What are the disadvantages of insulin pumps?
- difficulties learning to use the pump
- having it attached at all times
- blockages in the infusion set
- small risk of infection
How can T1DM be monitored?
HbA1c measures glycated haemoglobin, reflecting the average glucose level over the previous 3 months. It is measured every 3 to 6 months to track the average sugar levels.
Capillary blood glucose can be measured using a blood glucose monitor, allowing patients to self-monitor their sugar levels.
Flash glucose monitors use sensors that measure the glucose level of the interstitial fluid in the subcutaneous tissue. This means there is a 5-minute lag behind blood glucose, and so cannot be used if hypoglycaemia is suspected.
Continuous glucose monitors are similar to flash glucose monitors, but are attached constantly to allow continuous glucose monitoring.
What is acanthosis nigricans?
Thickening and darkening of the skin at the neck, axilla and groin.
Characteristic of insulin resistance.
