ENDOCRINOLOGY WK 5 Flashcards
common causes of hypoglycaemia
- Treatment
o Insulin
o Sulphonylureas
- Patient error o Too much insulin o Too little carbs o Missed/late meal o Exercise
- Alcohol
- (same for sulphonylureas) – eg gliclazide, glipizide
other less common causes of hypoglycaemia
- Decreased insulin requirement eg weight loss
- Liver disease, alcohol
- Conditions assoc. with T1DM
o Coeliac disease
o Addison’s disease (cortisol important counterregulation)
o Hypothyroidism
o Hypopituitarism - Complications of diabetes
o Autonomic neuropathy
o Injection sites/ lipohypertrophy
o Renal failure
o Counterregulatory failure
counter-regulation of hypoglycaemia
Glucagon – produced by alpha cells in pancreas
- Insulin and glucagon in balance in health
- Glucagon brings blood sugar up
Epinephrine
Cortisol (pro-longed)
Growth hormone (pro-longed)
why do hypoglycaemia symptoms change as diabetes progresses
- Changes in counterregulatory hormones over time
- Table below shows the % of deficiencies of counterregulatory hormones
- Lose glucagon response 100% by 5-10 yrs
- If you have diabetes for long have more neurological symtpoms because of this eg muddled instead of shaky
what symptoms do elderly diabetics get with hypoglycaemia and why
- When you’re older (had diabetes longer) epinephrine levels released at lower blood glucose levels
- Means you get a smaller peak of epinephrine
- Start to develop brain dysnfunction before hypoglycaemia
- Confused during hypo and so don’t know what to do = severe
what is the effect of having a hypo on risk in future
More hypos you have the less hormonal release you get
- Happening all the time so body doesn’t react as strongly
- Less warning you get = greater risk
diagnosis of hypoglycaemia
Whipple’s triad – 2 out of 3 - Typical symptoms - Biochemical confirmation (no agreed cut-off but 4mmol/l in general – this isn’t actually that low but is a good safety margin) - Symptoms resolve with carbohydrate Remember ‘atypical’ presentation esp in elderly - Hemiparesis In theory, confuirm w/ lab blood glucose - But don’t delay treatment
management of hypoglycaemia
- If alert – sweet drink or dextrose tablet
- If not alert – 20% dextrose iv
- If can’t access, give 1mg iv glucagon plus sweet drinl (not effective if alcoholic hypo)
- Follow up rapid acting carbs with slow release carbs
- 10% glucose infusion if long-acting insulin or SU
- If not recovering, consider other cause
- Full cognitive recovery can lag by 45 mins (driving)
- Glucagon injection
o Inject sterile water into powder, soak it back up and inject it
aftercare of hypoglycaemia
- Follow-up glucagon/ dextrose with a starchy snack
- Patients presenting to hospital with hypo are-
o Older
o Live alone
o Co-morbidity
o Sulfonylurea therapy - Discharge if make full recovery and responsible adult at home – not if sulfonyurea-induced
- Infrom the diabetes team
- Close monitoring of blood glucose for next 72 hours
- Was there an obvious remedial cause
- If not, cut right back on insulin
pathogenesis of Diabetic ketoacidosis
- Stop taking insulin
- glucose circulating but cells can’t take this up without insulin
- so most turn to other sources of energy…
o mobilise free fatty acids to make ketone bodies
o used as an alternative source of fuel when no glucose uptake - ketone bodies are acidic – cause metabolic acidosis
- as get rid of ketones in urine they cause an osmotic diuresis
o pee out lots of ketones which pulls out lots of water with it also
o makes you hypovolaemic
Other sources of fuel - break down muscles to make amino acids eg lactate and arginine
- plugged into gluconeogenesis cycle to make more glucose that we still can’t use
- extra glucose is peed out – water is taken with it – dehydration and decreased GFR
If you don’t have enough insulin but still some (aka Type 2 diabetes)
- switches off the fatty acid pathway so only breakdown of muscle instead
- so don’t become acidotic
- but have persistent cycle of high glucose > pee it out > dehyration
- but no acidosis
management of diabetic ketoacidosis
- Fluids > intitially fast then slower, to rehydrate
- Iv insulin > switch off ketone body production
- Monitor potassium – metabolic acidosis shifts K+ to extracellular space, as you give insulin, K+ moves into the cells and K+ falls
- Protocol driven
- Seek precipitant, commonly infection (inc. stress response inc. cortisol and GH) and errors/omissions
- Often no cause found
- In 10% of cases, DKA is first presentation of T1DM
diagnosis of diabetic ketoacidosis
- Polyuria, polydipsia
- Hypovolaemia
o JVP dec, BP dec, HR inc
o ~5L fluid deficit
o Sifnificant electrolyte deficit Na+, K+ and Cl- - Abdo pain, N&V
- Kussmaul resps, ketotic breath
- Muscle cramps
aftercare of DKA
- Swap to s/r isulin once patient eating and drinking
- Ensure basal insulin give > 1hr before iv insulin stops
- Try to identify precipitant
- Don’t miss oppprtunity for pt education
o Sick day rules
o Adjusting insulin - Involve DSN/ dietician, ensure F/U
- Look out for any complications
hyperosmolar hyperglycaemic syndrome (HONK)
- Usual finding is MARKED hyperglycaemia, raised osmolality and mild/no ketoacidsosis
- Mortality up to 33%
- 2/3 cases in previously undiagnosed DM
- Affects middle-aged or elderly type 2 DM
diagnosis of HONK
- Hyperglycaemia (>30mmol/l, but often 60-90 mmol/l)
- Serum osmolality >320mmol/Kg
- No/mild ketoacidosis
- Severe dehydration and pre-renal failure common
Calculated osmolarity = 2x (Na + K) + glc + urea - If above 320 = hyposmolar hyperglycaemic
presentation of DKA
- Insidious onset
- Profound dehydration (9-10L) deficit
- Hypercoagulability (exclude CVA, DVT, PE)
- Confusion, coma, fits
- Gastroparesis, N&V, haematemesis
management of DKA
- Slower, prolonged rehydration (older, underlying heart disease etc)
- Gradual reduction in Na+
- Gentler glucose reduction
- Anticoagulation vital – prophylactiv sc Heparin
- Seek the precipitant (infection, MI etc)
lactic acidosis and metformin use
- Evidence that MF causes lactic acidosis is poor
- It does not increase lactate levles in T2DM
- Short t1/2 so rarely accumulates in absence of advanced RF
- Usually, tissue hypoxia is ‘trigger’
- Review of cases of MF-associated lactic acidosis 1995-2000 showed no cases were caused solely by MF
- Cochrane review 2002 concluded that treatment with MF not assoc. with inc. risk of LA
when to stop metformin to prevent lactic acidosis
- Stop MF if eGFR <30 (or worsening fast)
- Withdraw during tissue hypoxia but can reinstate later
o Shock
o MI, significant CCF
o Sepsis
o Dehydration
o Acute renal failure - Withdraw for 3 days after iodine-containing contrast medium given
o Check U/E before reinstating 48h later - Withdraw 2 days before general anaesthetic and reinstate once renal function stable
making a diagnosis of diabetes in childhood
MAKING AN EARLY DIAGNOSIS - THINK – symptoms (4 x Ts) o Toilet – using more o Thirsty o Thinner o Tired - TEST – immediately o Finger prick capillary glucose test o If result >11mmol/l - TELEPHONE urgently o Contact your local specialist team for a same day review
presentation of diabetes in children
- Glucose is a powerful osmotic agent
- Subsequent polyuria and secondary polydipsia
Nocturnal enuresis Dehydration Weight loss - Insulin is an anabolic hormone so in absense of insulin body is catabolic state breaking down its muscle mass contributing to weight loss Lethargy and behavioural changes Blurred vision Vaginal candidiasis
insulin treatment in children with diabetes
- Must be started as soon as possible after diagnosis (usually within 6 hours if ketonaemia is present)
- Children can develop dehydration + acidosis within 24 hours of first presentation
o Children < 2 yrs old are more at risk - This is to prevemt metabolic decompensation and diabetic ketoacidosis
ketone metre - uses and interpretation
- Put blood on a strip
- Normal ketone reading – 0.1-0.2
- Can be higher if haven’t eaten in a while (0.3)
- Ketone reader reads up to 8mmol/l over this registers as HI
- Reading of 3 is likely to develop ketoacidosis
- But DKA can’t be diagnosed solely from this reading
common causes of DKA in children
DKA is the result of an absolute or relative deficiency of insulin
- Newly diagnosed diabetes
o In children with established TIDM – the risk is 1-10% per patient per year
o Infections
o Non compliance with treatment (75%). Children whose insulin is administered by a responsible adult rarely get DKA
o Insulin pump therapy – no background insulin circulating
Begin to develop ketones in 6 hours
Because no inhibition by insulin of hormone sensitive lipase
pathophysiology of DKA - how it affects/ presents in children
- An accelerated catabolic state, impaired peripheral glucose utilization, increased lipolysis + ketogenesis
- Hyperglycaemia + hyperketonaemia cause osmotic diuresis + dehydration
- Dehydration becomes a major feature
o Vomiting in children with diabetes is a sign of insulin deficiency until proven otherwise
o Hyperglycaemia and hyperetonaemia causes a degree of gastric stasis and gut iylias
o So indiv. Cont. to want to drink whilst in DKA
o Fluid unable to process fluid load in stomach and so instead vomit due to lack of movement through the gut - Lactic acidosis from hypoperfusion
clinical presentation of DKA - symptoms and biochemistry in children
- Dehydration
- Nasusea, vomiting and abodminal pain, mimicking an acute abdomen
- Acidotic respiration (kussmaul) deep + sighing
- Altered conscious level
Biochemical data - pH <7.3 +/or bucarbonate <15mmol/L
- base excess – strongly negative
- high anion gap
- hyperglycaemia
- hyperketonaemia
key aims of paediatric DKA
- meticulous monitoring of clinical condition of the patient and the biochemical data
- correct dehyrdation slowly (over 48 hours in those < 18 yrs)
- correct acidosis slowly + reverse ketosis – iv insulin infusion and NOT bicarbonate therapy
- restore BE to near normal
- avoid complication of therapy – paediatric cerebral oedema
education plan for newly diagnosed child
ward based – basic education
o admit all young people with new diabetes diagnosis to the ward
o commence basal bolus insulin regimen
- home based – social issues
- school/ nursery visits
o on insulin regimens – require diabetes care throughout skl/ nursery day
Clinic based – on-going package of care
- new patient clinic
- review pateint (at review patient see patient 3-4 months)
- young person’s clinic (aged 16-18 yrs)
aims of sick day management
- Do not omit insulin > always check blood ketone value
- Switch off ketogenesis (requires additional insulin)
- Ensure sufficient carbohydrate substrate is available
- Achieve normoglycaemia
o Febrile patients generally have an increased insulin requirement (25-50%)
o Patient with D+V within no ketonaemia may have a reduced insulin requirement (20% in each dose) - Altered insulin doses may be required for up to one week after intercurrent illness
- Treat current illness
HbA1c targets for children and young people
- Explain to children and young people with type 1 diabetes that their families or carers
o That an HbA1c level of 48mmol/mol or lower will minimise their risk of long term complications
o Who have an HbA1c level above 48mmol/mol that any reduction in levels reduces that risk
how does blood glucose effect HbA1c values in 3/4 months
- Day 1-6 > very low contribution
- Day 7-30 > 50%
- Day 31-60 > 25%
- Day 61-90 > 15%
- Day 90-120 > 10%
Time in range to measure glycaemic control
Precentage of time % that a person spends within their target glucose range, usually 3.9-10mmol/l
Time below range is the percentage of time spne tbelow 3.9mmol/l
Produced by libre data (continuous glucose monitoring)
time in range and how it relates to HbA1c - targets
- Direct relationship between HbA1c and time in range
o The higher the time in range the lower the HbA1c - The clinic TIR (time in range) target is a70% as strongly correlates with an HbA1c of 53mmol/mol
- It is also important to look at time below range
o Recommeneded TBR below 4% - Important to note that what may appear small success ie 5% increase in TIR is significantl imporving glycaemic control
barriers to achieving glycaemic contorl
- Day to day family life
- Fear of hypoglycaemia and seizures
- School day
- Activitie / exercise / holidays
- Insulin omission
- Fave injection sites – lipohypertrophy
- Diabulimia (deliberate insulin omission to lose weight)
insulin injection sites
stomach
thigh
bottom
- not in arms because not enough subcutaenous fat
insulin pumps - availability, why teenagers need them
- Scottis govt. funding
- Current patient on pumps 266 (59.5%)
Why should get an insulin pump as a teenager… - Don’t want to avoid exercise
- Don’t want to feel different from friends
- Want to feel like a normal teenager again
