Diabetes Flashcards
WHO definition of diabetes
“Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys and nerves”
A group of conditions where the body cannot produce enough or any insulin, cannot properly use the insulin that is produced, or cannot do a combination of either.
What are the 7 main types of diabetes?
Type 1 - life changing and lifelong
Type 2 - can be put into remission, more aggressive in children and high complication risk at diagnosis
MODY – rare form of diabetes, runs in families, caused by a single gene mutation with 50% inheritance. Not necessarily needing insulin and can be treated with sulphonylureas
Neonatal - rare form diagnosed in under 6 mths of age. Transient or permanent, but if transient usually recurs later on in life. Treated with Glibenclamide, sulphonylurea
Wolfram (DIDMOAD – DI, DM, optic atrophy and deafness, rare autosomal recessive)
Alstrom – rare genetic disorder, progressive loss of hearing and vision, obesity, short stature, T2
Gestational Diabetes – high blood sugar (glucose) that develops during pregnancy and usually disappears after giving birth. Risk factors high BMI, previous GDM, S Asian, Black, Afro-Carribean, Middle Eastern origin, FH diabetes. It can happen at any stage of pregnancy, but is more common in the second or third trimester.
LADA – latent autoimmune diabetes in adults (type 1 ½), seems to straddle elements of T1 and T2
Others – include secondary causes such as CF related diabetes, thalassaemia
What is the incidence of T1 diabetes in children
UK has the highest number of children aged 0-14 years with T1DM in Europe
Incidence of Type 1 diabetes increased significantly in 2020/21 amongst those aged 0-15, from 25.6 new cases per 100,000 in 2019/20 to 30.9 in 2020/21 – an increase of 20.7% (p<0.001).
The estimated prevalence rate of Type 1 diabetes in England and Wales was 204.5 per 100,000 of the general population.
2 peaks of incidence – 4-5 year olds, and 10-11 year olds
Risk factors – family history, genetics, geography and age
Autoimmune destruction of the insulin producing pancreatic beta cells, assoc with HLA types DR3 and DR4
Environmental and viral triggers on a genetically susceptible background
Presenting features – polyuria, polydipsia, weight loss and tiredness
4 Ts of T1 diabetes
Toilet
Thirst
Tired
Thinner
T1 generally an acute presentation via GP or ED
Symptoms described may be non-specific
Must be same day referral to hospital
May present compensating, or in DKA
Diagnosis should never be made based on waiting for OGTT or HbA1c
T2 diabetes in children
Incidence is rising
Very aggressive disease and worse prognosis than T1
At presentation, 44% already have hypertension, and 25% have kidney disease
In 2000, no recorded children in UK with T2DM
In 2015 0.72 / 100 000
In 2019/20 NPDA report, 866 cases in CYP
In 2020/21 NPDA report, 973 cases
The numbers diagnosed between the two years had shown a 14% increase, in the same timeframe as a 20% increase in overweight and obesity
Risk factors – obesity, girls, non-white ethnicity and deprivation
The response to insulin is diminished, producing insulin resistance, initially countered by an increase in insulin production to try and maintain glucose homeostasis.
Diagnosis often made on OGTT
More insidious presentation, usually asymptomatic, may have outward signs of insulin resistance such as acanthosis nigricans, and therefore screened
Prevalence of diabetes types
Type 1 – 97%
Type 2 – 1.5%
Other – 1.5% - MODY, secondary diabetes
What is needed for a diabetes diagnosis?
Diabetes symptoms plus:
a random venous plasma glucose concentration ≥ 11.1 mmol/l or
a fasting plasma glucose concentration ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l) or
two hour plasma glucose concentration ≥11.1 mmol/l two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).
How do we give a diagnosis if there is no symptoms?
With no symptoms diagnosis should not be based on a single glucose determination but requires confirmatory plasma venous determination. At least one additional glucose test result on another day with a value in the diabetic range is essential, either fasting, from a random sample or from the two hour post glucose load
What HbA1c is needed for diabetes?
A venous HbA1c of 48mmol/mol (6.5%) is the cut off point for diagnosing diabetes. A value of less than 48mmol/mol (6.5%) does not exclude diabetes diagnosed using glucose tests.
Pre-diabetes for T2 – HbA1c 42-48mmol/mol
What is the initial management for T1 not in DKA?
Insulin treatment
Commence on 0.5-0.8 Units/kg/day
Approx 50% given as long acting insulin
And 50% as rapid acting for meals (10% breakfast, 20% lunch, 20% tea)
Pen therapy is usual initial treatment, converting to pump therapy if indicated /appropriate
Fixed doses to start with and then carb counted meals with a set insulin:carbohydrate ratio (ICR)
Insulin sensitivity factor for correction doses (ISF), based on total daily dose of insulin and 100 rule
Blood glucose testing at least 5 times a day, pre-meals, pre bedtime, exercise, feeling unwell and post-prandial
CGMS / FGMS
Advantages of DKA
accuracy, no time lag
Advantages of continuous glucose monitoring system
Glucose trends, alarms for highs and lows, ‘follow’ facility for carers and teachers, can communicate with pump delivery systems, less trauma to fingers
What are the signs of DKA?
Nausea and vomiting
Abdominal pain
Hyperventilation
Dehydration
Reduced level of consciousness
DKA severity values
MILD – pH < 7.3 or plasma bicarbonate <15 mmol/l
MODERATE – pH <7.2 or plasma bicarbonate < 10 mmol/l
SEVERE – pH < 7.1 or plasma bicarbonate < 5 mmol/l
One to one nursing or HDU if under 2 years or severe DKA
What are the blood gases for DKA?
pH 7.06
pCO2 2.8
BE – 15
HC03 13
What happens when there is insulin deficiency + glucagon excess?
Inc Blood ketones and Inc Blood glucose
Inc blood ketones leads to vomiting
Inc both of them leads to osmotic diuresis
vomiting + osmotic diuresis causes fluid and electrolyte depletion
Blood ketones inc leads to acidosis
Acidosis leads to cellular dysfunction
fluid and electrolyte depletion leads to cerebral oedema and shock
What does insufficient insulin cause?
Rising glucose, plus released from stores
Glucose released in urine with fluid, urine output increases
Thirst+++, dehydration
Rising ketones (fat broken down to release energy
Blood becomes acidic
Ketones excreted in urine, breathed out from lungs, vomiting, unwell
What is the management of DKA
Fluid
Insulin
Monitor glucose hourly
Monitory electrolytes, especially K+ and ketones -2-4 hourly
Very strict fluid balance - hourly I/O
Hourly neuro obs
(New diagnosis bloods)
How do we break the vicious cycle?
Fluids first to rehydrate
Insulin is required to ‘switch off’ ketone production, start 1-2 hrs after fluids
Low dose continuous infusion 0.05-0.1 units/kg/hr
Aim for slow reduction in blood glucose
What to watch out for in DKA?
cerebral oedema
shock
hypokalaemia
aspiration
thrombus
What is given for fluid in DKA and how do we calculate how much fluid is needed?
If clinically dehydrated but not in shock give an initial IV 10ml/kg bolus of normal saline over 30 min
When calculating total fluid requirement, subtract this bolus from total fluid deficit
Is shocked (weak, thready pulse, hypotension, give an initial bolus of 20ml/kg.
When calculating total fluid requirement, do not subtract this fluid bolus from the total fluid deficit
Assume a 5% fluid deficit in children and young people in mild to moderate DKA (pH 7.1 or above)
Assume a 10% fluid deficit in children and young people in severe DKA (pH < 7.1)
Give normal maintenance fluids + correct the deficit
Correct for dehydration over 48 hours
Patient is 26kg and dehydrated
26 kg
10% dehydrated = 2600 ml)
2600 / 48 hours = 54 ml/hr
Maintenance
100ml/kg for first 10kg of BW
50ml/kg for second 10kg of BW
20ml/kg for every kg after this
(use maximum weight of 75kg)
1000ml + 500ml +120ml = 1620ml
68 ml/hr
Total
122 ml/hr
Initial treatment for Type 2 diabetes
Metformin +/- Insulin therapy
Consideration of GLP- 1 agonists – Liraglutide (>10 years), Semaglutide (> 18 years)
Diet - Calorie / carb reduction – weight loss
Lifestyle – physical activity, sleep, screentime
What are the blood glucose targets in T1 and T2?
Pre –meal BG – 4-7mmol/l
Pre bedtime BG 5-8mmol/l
Post prandial BG <10mmol/l
Average BG <7mmol/l
Time in range (4-10mmol/l) >70%
Time hypo (<4mmol/l) < 4%
HbA1c <48mmol/mol
Quicker these targets are achieved after diagnosis and longer they are sustained, prolongs ‘honeymoon’ period of endogenous insulin secretion, and better long term outcomes with metabolic memory
How do we calculate how much insulin to give?
Insulin to carbohydrate ratio
1 unit for every 15 grams
Correction factor
1 unit to bring blood glucose down by 8 (aiming for a BG of 6)
How many doses do you need for 50 grams of fusilli carbohydrate?
Current blood glucose
14.2 mmol/l
Insulin to carbohydrate ratio
1 unit for every 15 grams
Eating 17g of CHO = 1 unit of insulin
Correction factor
1 unit to bring blood glucose down by 8 (aiming for a BG of 6)
Correction dose = 1 unit
Total dose = 2 units
S + S of autonomic hypoglycaemia
Irritable
Hungry
Shaky
Anxious
Sweaty
Palpitations
Pallor
S + S of neuroglycopenic hypoglycaemia
Confused
Drowsy
Hearing or visual problems
Headache
Slurred speech
Unusual behaviour / moodiness
Coma
Seizures
Hypo management mild/ moderate
Check blood glucose to confirm
glucose tablets
glucose gel
glucose containing food or drink (not chocolate!)
Check BG in 15 minutes
Follow up with longer acting carb (bread/biscuit)
What does diabetic retinopathy cause in the eye?
Haemorrhages
Abnormal growth of blood vessels
Aneurysm
Cotton wool spots
Hard exudates
Diabetes in infancy?
Rare – sometimes transient
Very sensitive to insulin
Frequent small milk feeds
Practical problems of testing and injections
Risks of hypoglycaemia vs risk of longstanding diabetes
Toddler diabetes features
Food – tend to graze, small meals little and often
Behavioural issues – eating, injections, tests
Hypos – may be difficut to recognise
Hypos may affect neurodevelopment
School age diabetes features
Increasing independence
Food – making own choices, school dinners
Effect of exercise – PE, playground, after school activity, clubs, and team sport
Behaviour and compliance
Sleepovers
School residentials and trips
Adolescence and diabetes
This group have the poorest glycaemic control
Non-compliance
immortal
risk taking
weight manipulation
sex / drugs / alcohol
Insulin resistance
