diabetes type 1 Flashcards
explain the pathology behind type 1 diabetes?
- pancreas stops being able to produce adequate insulin
- glucose isn’t taken up into cells so they think there’s no glucose available
- however, glucose levels in blood keep rising causing hyperglycaemia
what does type 1 diabetes present with?
- classical triad of symptoms of hyperglycaemia ( polyuria, polydipsia, weight loss)
- diabetic ketoacidosis
whats the underlying cause of type 1 diabates?
unclear
certain viruses may trigger it
whats the ideal blood glucose concenration?
4.4-6.1mmol/L
what process does insulin cause?
glycogenesis
what process does glucagon cause?
gluconeogenesis
explain the role of glucagon in glucose metabolism?
- alpha cells - islets of langerhans
- catabolic
- released in response to low blood glucose and stress
- tells liver to break down glycogen and releases it into the blood as glucose - glycoenolysis
- also tells liver to convert proteins and fats into glucose - gluconeogenesis
explain the role of insulin in glucose metabolism?
- hormone
- beta cells - islets of langerhans
- anabolic
- reduces blood sugar in 2 ways
- causes bodily cells to absorb glucose
- causes cells to store it as glycogen
explain the role of ketones in metabolism?
- released when low glucose stores
- made by the liver
- made from long chain fatty acids
- water soluble
- can cross blood-brain barrier
how can ketone levels be measured?
- urine - dipstick test
- blood - ketone meter
- acetone smell breath
what is the most common scanario for diabetic ketoacidosis to occur?
- type 1 diabetes
- type 1 diabetic with other illnesses eg infection
- type 1 diabetic who isnt sticking to their insulin regeime
what are the 3 key features for diabetic ketoacidosis?
- ketoacidosis
- dehydration
- potassium imbalance
the 3 key features of diabetic ketoacidosis are ketoacidosis, dehydration and potassium imbalance, explain why the ketoacidosis is present?
- without insulin body cells dont recognise glucose even tho its there in the blood
- liver will then start to produce ketones
- the kidney produces bicarb to buffer these but they get used up making the blood acidic
the 3 key features of diabetic ketoacidosis are ketoacidosis, dehydration and potassium imbalance, explain why the dehydration is present?
- hyperglycaemia overwhelmes the kidneys
- glucose leaks into the urine
- this pulls water with it
- causes polyuria and polydipsia
the 3 key features of diabetic ketoacidosis are ketoacidosis, dehydration and potassium imbalance, explain why the potassium imbalance is present?
- insulin normally drives potassium into cells
- no insulin so little potassium in cells
- blood potassium can either be high or normal bc the kidneys balance it
- however total body potassium is low because it isnt in cells
- patients develop hypokallaemia v quickly qhich can lead to arrhythmias
what is the pathophysiology of diabetic ketoacidosis?
- hyperglycaemia
- dehydration
- ketosis
- diabetic acidosis (with a low bicarb)
- potassium imbalance
what are the symptoms of diabetic ketoacidid?
- polyuria
- polydypsia
- nausea and vomitting
- acetone smelling breath
- dehydration
- weight loss
- hypotension
- altered consciousness
what is the diabetic ketoacidosis diagnosing criteria?
- hyperglycaemia - blood glucose over 11mmol/L
- ketosis - blood ketones above 3mmol/L
- acidosis - PH below 7.3
what are the most dangerous parts of diabetic ketoacidosis and therefore what is the treatment priority?
- dangerous - dehydration, potassium imbalance, acidosis
- priority - fluid resuscitation - insulin infusion
what are the principles of management and whats the nemonic?
FIG-PICK
F - fluids - IV fluid with normal saline - 1L in the first hour followed by 1L every 2 hours)
I - insulin - fixed rate insulin infusion
G - glucose - add glucose when less than 14mmol/L
P - potassium - ass potassium to IV
I - infection - treat underlying infections
C - chart fluid balance
K - ketones - monitoe blood ketones, PH and bicarb
what must you ensure is true before stopping the insulin and fluid infusions?
- ketones and acidosis should have resolved
- they should be eating and drinking
- they should have started their regular subcutaneous insulin
what are the key complications during treatment?
- hypoglycaemia
- hypokalaemmia
- cerebral oedema
- pulmonary oedema
what can be used to assess if a patient has type 1 or type 2 diabetes?
autoantibodies and serum-c peptide
autoantibodies present in a type 1 diabetic are:
- anti-islet cell antibodies
- anti-GAD antibodies
- anti-insulin antibodies
serum-c peptode is a measure of insulin production - if lots then lots
what components are involved in the long-term management of type 1 diabetes?
- subcutaneous insulin
- monitoring dietary carbohydrate intake
- monitoring blood sugar levels upon waking, at each meal, and before bed
- monitoring for and managing complications, both short and long term
what are the different ways of managing insulin artificially?
- basal-bolus reegime
- insulin pumps
- pancreas/islet transplant
- monitoring
- closed-loop system
explain what the basal-bolus regime is?
combo of:
- background, long acting insulin injected once a day
- short-acting insulin inhjected 30 mins before consuming carbs
what is the issue with always injecting into the same spot?
- lipodystrophy - subcutaneous fat hardens and dont absorb insulin properly
- cycle the injection sites
explain what an insulin pump is and list the different types?
- pumps that continuously infuse insulin at diff rates to control sugar levels
- pushes insulin through a cannula
- cannula replaced every 2-3 days
types:
tethered pump
patch pump
what are the advantages and disadvantages of insulin pumps?
advantages:
- better blood sugar control than basal-bolus
- more flexibility with eating
- less injections
disadvantages:
- difficulties learning to use the pump
- having it attached all the time
- blockage of infusion set
- small risk of infection
describe the differences between tethered and patch pumps?
tethered pumps:
- replacable infusion sets and insulin
- attached to patients belt
- controls of pump itself
patch pumps:
- on skin with no tubes visible
- replaced when insulin runs out
- remote controlled
what does a pancreas transplant involve?
- implanting a donor pancreas to produce insulin
- original pancreas is left in place to produce digestive enzymes
- carries significant risks and life -long immunosuppressio is required to prevent rejection
what does islet transplantation involve?
- donor islet cells into patients LIVER
- cells will then produce insulin
- patients still usually need insulin therapy after
whats the role of HbA1c in measuring?
- measures glycated haemoglobin
- this is how much glucose is attached to the haemoglobin molecule
- reflects the average glucose level over previous 2-3 months
- measured every 3-6 months
what are the different methods of glucose monitoring?
- capillary blood glucose
- flash glucose monitors
- continuous glucose monitor
what is a capillary blood glucose monitor?
- finger prick test
- can be measured using a blood glucose monitor
- gives an immediate result
- patients with type 1 and type 2 diabetes rely on these
- self-monitoring
what is the flash glucose monitor?
- sensor on the skin that measures the glucose level of the interstitial fluid in the subcutaneous tissue
- 5-min lag
- records at short intervals over time
- need to swipe mobile phone over sensor
- sensor needs replacing every 2 weeks
what is the continuous glucose monitor?
- similar to flash glucose monitor
- don’t need to scan sensor - the results are sent over via bluetooth
what is the closed loop system / artificial pancreas?
- combo of continuous glucose monitor and insulin pump
- the devices communicate to automatically adjust insulin based off the glucose readings
- patients still need to input carb intake and adjust the system for exersize
what are the short-term complications to immediate insulin and blood glucose management?
- hyperglycaemia and diabetic ketoacidosis
- hypoglycaemia
what are the causes of hypoglycaemia?
- too much insulin
- not enough carbs
what are the symptoms of hypoglycaemia?
- hunger
- tremor
- sweating
- irritability
- dizziness
- pallor
severe: - reduced consciousness
- coma
- death
how is hypoglycaemia treated?
- rapid acting glucose
- once it improves they consume slow acting carbs
- severe: - IV dextrose and intramuscular glucagon
how is hyperglycaemia treated?
- doesnt acc nessasarily need treating
- insulin takes a while to take effect and too much can cause hypoglycaemia
what are the 3 main catagories of long term complications of chronic high blood sugar and why does this happen?
- chronic high blood glucose causes damage to endothelial cells of blood vessels
- causes them to become leaky
- makes them unable to regenerate
catagories:
- macrovascular
- microvascular
- infection - related
what are the macrovascular long-term complications?
- coronary artery disease
- peripheral ischemia
- stroke
- hypertension
what are the microvascular long term complications?
- peripheral neuropathy
- retinopathy
- kidney disease - nephropathy
what are the infection-related long term complications?
- urinary tract infections
- pnemonia
- skin and soft tissue infections, particularly in feet
- fungal infections, particularly oral and vaginal candidiasis
At what level of Beta cell destruction does hyperglycaemia develop?
80-90%
At what level of blood glucose can it no longer be absorbed?
10mmol/L
Thirsty and develop polyuria - body attempts to remove excess glucose
Diagnosis of T1DM (3)
Random blood glucose ≥11.1mmol/L
Fasting blood glucose ≥7mmol/L
HbA1c ≥ 48mmol/mol
- One abnormal result in symptomatic patients is sufficient
- Two abnormal results needed in asymptomatic patients on 2 different days
Environmental factors that can increase the risk of developing T1DM (4)
- Diet
- Vitamin D deficiency
- Early-life exposure to viruses associated with islet inflammation (eg: enteroviruses)
- Decreased gut-microbiome diversity
Epidemiology of T1DM (4)
- Young (usually between 5-15 years)
- Lean
- North European descent
- 10% of diabetes is type 1
First line treatment for T1DM (2)
Basal-Bolus regimen of Insulin
Basal - Long acting (either given twice or once daily)
Bolus - Short acting before meals
How can T1DM be differentiated from Latent Autoimmine Diabetes in Adults (LADA)? (2)
- In LADA age of onset is >30 yrs
- Low to normal C-peptide
how does type 1 diabetes differ from monogenic diabetes?
In type 1 diabetes:
- C-peptide present
- Autoantibodies absent
How can T1DM be differentiated from Neonatal diabetes?
neonatal occurs in first 6 months of life
due to genetic mutation - testing
NICE diagnostic criteria for T1DM (6)
- Clinical features and evidence of hyperglycaemia
- Ketosis
- Rapid weight loss
- < 50 years
- BMI < 25 kg/m2
- Personal and/or family history of autoimmune disease
Other autoimmune conditions that can result from T1DM (most to least common) (6)
- Thyroid disease
- Autoimmune gastritis
- Pernicious anemia
- Coeliac disease
- Vitiligo
- Addison’s disease
Signs of T1DM (6)
- BMI < 25kg/m2
- Failure to thrive in children
- Glove and stocking sensory loss
- Reduced visual acuity
- Diabetic retinopathy
- Diabetic foot disease
What is a Mixed insulin regimen? (3)
- A mixture of short or rapid acting and intermediate-acting insulin
- Twice daily
- For those who can’t tolerate multiple injections for basal bollus
what is continuous insulin for?
- If patient has disabling hypoglycaemia
- or persistently hyperglycaemic (HbA1c > 69mmol/mol) on multiple injection insulin therapy
Which genes are linked with increased risk of developing T1DM? (4)
HLA-DR2 and HLA-DQ3
or
HLA-DR4 and HLA-DQ8
