Diabetes Flashcards
(34 cards)
Type 1 diabetes
Pancreas stops being able to produce adequate insulin
Without insulin, the cells cannot absorb glucose from the blood and use it as fuel & therefore think no glucose is available, whilst glucose level keeps rising = hyperglycaemia
Type 1 diabetes classic triad symptoms
Polyuria
Polydipsia
Weight loss
Ketogenesis
Occurs when there is insufficient glucose supply and glycogen stores are exhausted
Liver takes fatty acids and converts them to ketones (water-soluble fatty acids)
Can cross the BBB and be used by the brain
Level can be measured in the urine with a dipstick and in the blood using a ketone meter, people in ketosis = acetone smell to their breath
Kidneys buffer ketone acids in healthy people, so blood does not become acidotic
Diabetic ketoacidosis pathophysiology
1) Ketoacidosis – without insulin, cells cannot recognise glucose, so liver starts producing ketones to use as fuel; over time there are high glucose and ketones levels; initially kidneys produce bicarbonate to counteract the ketone acids in the blood & maintain normal pH; over time, ketone acids use up the bicarbonate & blood becomes acidic
2) Dehydration – hyperglycaemia overwhelms the kidneys and glucose leaks into the urine, glucose in the urine draws water out by osmotic diuresis -> polyuria and severe dehydration -> polydipsia
3) Potassium imbalance – when treatment with insulin starts, patients can develop severe hypokalaemia very quickly, leading to fatal arrhythmias
Diabetic ketoacidosis symptoms
Polyuria
Polydipsia
N&V
Acetone smell to their breath
Dehydration
Weight loss
Hypotension
Altered consciousness
DKA diagnosis
Hyperglycaemia (BM>11)
Ketosis (blood ketones > 3 mmol/L)
Acidosis (pH < 7.3)
DKA treatment
Priority is fluid resuscitation to correct dehydration, electrolyte disturbance and acidosis
Followed by insulin infusion to get the cells to start taking up and using glucose and stop producing ketones
F – fluids
I – insulin (fixed rate insulin infusion)
G – glucose (closely monitor BM and add a glucose infusion when it is less than 14)
P – potassium (add K+ to IV fluids)
I – infection (treat underlying triggers such as infection)
C – chart fluid balance
K – ketones
DKA treatment complications
Hypoglycaemia
Hypokalaemia
Cerebral oedema, particularly in children
Pulmonary oedema (secondary to fluid overload/acute respiratory distress syndrome)
Type 1 diabetes long-term management
Subcutaneous insulin
Monitoring dietary carbohydrate intake
Monitoring blood sugar levels upon waking, at each meal & before bed
Monitoring for and managing complications, both short and long term
Insulin pumps
Small devices that continuously infuse insulin at different rates to control blood sugar levels
Pump pushes insulin through a small plastic tube (cannula) inserted under the skin
Cannula is replaced every 2-3 days & insertion sites are rotated to prevent lipodystrophy and absorption issues
Insulin pumps pros and cons
P – better blood sugar control, more flexibility with eating & less injections
C – difficulties learning to use the pump, having it attached at all times, blockages in the infusion set, small risk of infection
Tethered vs patch pumps
Tethered – devices with replaceable infusion sets and insulin, usually attached to the patient’s belt/around the waist with a tube connecting the pump to the insertion site, controls are on the pump itself
Patch – sit directly on the skin without any visible tubes, entire patch pump is disposed of when insulin runs out, a separate remote usually controls patch pumps
Type 1 diabetes transplant
Pancreas transplant – implanting a donor pancreas to produce insulin
- Original pancreas is left in place to continue producing digestive enzymes
- Life-long immunosuppression is required to prevent rejection so reserved for patients with severe hypoglycaemic episodes & those having kidney transplants
Islet transplantation – inserting donor islet cells into the patient’s liver -> produce insulin
- Patients often still need insulin therapy after islet transplantation
Type 1 diabetes monitoring
HbA1c
Capillary blood glucose
Flash glucose monitors – use a sensor on the skin that measures the glucose level of the interstitial fluid in the subcutaneous tissue, 5-minute lag behind blood glucose, need replacing every 2 weeks, 5-minute delay means it is necessary to do CBG testing if hypoglycaemia is suspected
Continuous glucose monitors – similar to flash but send readings over Bluetooth so patient is not required to scan the sensor
T1DM closed-loop system
Artificial pancreas
Combination of a continuous glucose monitor and an insulin pump
Devices communicate to automatically adjust the insulin based on the glucose readings
Patients still need to input carb intake & adjust the system to account for strenuous exercise
T1DM short-term complications
Hypoglycaemia – caused by too much insulin, not consuming enough carbs or not processing carbs correctly (malabsorption, diarrhoea or vomiting)
- Symptoms: hunger, tremor, sweating, irritability, dizziness and pallor; severe = reduced consciousness, coma and death unless treated
Hyperglycaemia – may indicate that the insulin dose needs to be increased, short episodes of hyperglycaemia do not necessarily require treatment (insulin injections can take several hours to take effect & repeated doses = hypoglycaemia), essential to exclude diabetic ketoacidosis
T1DM long-term complications
Chronic high glucose causes damage to the endothelial cells of blood vessels
Leads to leaky, malfunctioning vessels that are unable to regenerate
Immune system dysfunction and create an optimal environment for infectious organisms to thrive
Macrovascular – coronary artery disease, peripheral ischaemia (diabetic foot ulcers), stroke, hypertension
Microvascular – peripheral neuropathy, retinopathy, kidney disease (glomerulosclerosis)
Infection – UTI, pneumonia, skin and soft tissue infections, fungal infections (oral and vaginal candidiasis)
T2DM
Combination of insulin resistance and reduced insulin production cause persistently high blood sugar levels
More and more insulin is required to stimulate the cells to take up and use glucose -> pancreas becomes fatigues and damaged by producing so much insulin & insulin output is reduced
T2DM risk factors
Non-modifiable – older age, ethnicity (black, south Asian), family history
Modifiable – obesity, sedentary lifestyle, high carbohydrate
T2DM symptoms and signs
Tiredness
Polyuria and polydipsia
Unintentional weight loss
Opportunistic infections
Slow wound healing
Glucose in urine
Acanthosis nigricans – thickening and darkening of the skin often at the neck, axilla and groin, often associated with insulin resistance
Pre-diabetes
Indication that the patient is heading towards diabetes
Do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes
HbA1c of 42-47 indicates pre-diabetes
T2DM diagnosis
HbA1c > 48 mmol/mol or above indicated type 2 diabetes
Sample typically repeated after 1 month to confirm the diagnosis
T2DM management
Structured education program
Low-glycaemic-index, high-fibre diet
Exercise
Weight loss if overweight
Antidiabetic drugs
Monitoring and managing complications
T2DM treatment targets
48mmol/mol for new T2DM
53mmol/mol for patients requiring more than one antidiabetic medication
