C - Hypoglycaemia Flashcards
what key factor does treatment of hypoglycaemia depend on
whether pt is conscious or not
Mx of hypoglycaemia for alert and orientated pt
oral carbs
rapid acting: juice / sweets
longer acting: sandwich
Mx of hypoglycaemia for drowsy / confused with a good swallow pt
buccal glucose
rapid acting: eg hypostop / glucogel
longer acting: IV access ?
Mx of hypoglycaemia for unconscious pt or poor swallow pt
IV access
20% glucose IV
Mx of hypoglycaemia if deteriorating / refractory / insulin induced / difficult IV access
IM / SC img glucagon
what must be simultaneously done when Tx hypo
continuous monitoring
- keep rechecking the glucose
what can extravasation of glucose cause
irritation and phelbitis
how long does glucagon take to work and why
15-20 mins
mobilised glycogen stores
what is the danger of using glucagon
rebound hypoglycaemia
who can’t be given glucagon and why
liver failure pts
- no glycogen stores to mobilise
define hypoglycaemia in terms of glucose level
hard to say
- on wards: BM below 4 mmol/L
- sometimes below 3.5
what is a worrying blood sugar in a neonate
2.5
symptoms of hypoglycaemia
can be none
adrenergic: tremor, palpitations, sweating, hungry
neuroglycopaenic: somnolence, confusiom, incoordination, seizures, coma
what is it called when you get no symptoms of hypoglycaemia
loss of hypoglycaemia awareness
who gets loss of hypoglycaemia awareness
people who are having frequent hypos (insulin T1DM)
what 3 factors define hypoglycaemia
low glucose
symptoms
relief of symptoms with glucose administration
what is the first physiological response to low glucose
pancreas stops making insulin & starts making glucagon
what is the effect of the body reducing insulin and producing glucagon in response to low glucose
reduced peripheral uptake of glucose
increased glycogenolysis
increased gluconeogenesis
increased lipolysis
where is glycogen stored
liver
what is glycogen
store of glucose
what is gluconeogenesis
production of glucose from amino acids
how are ketones produced in response to low glucose
low glucose
–> reduced insulin production and increased glucagon production in pancreas
–> increased lipolysis
–> increased free fatty acids
–> beta oxidation (ATP generation from burning FFAs in mitochondria)
–> increased ketone body production
are ketones formed when even small amounts of insulin are circulating
NO - only formed when insulin suppressed
what is a later response of the body to low glucose
low neuronal glucose sensed by hypothalamus
–> sympathetic activation producing catecholamines
also
–> ACTH, cortisol, GH production
how do you diagnose hypoglycaemia in healthy people
conduct a prolonged fast to demonstrate it
gold standard way of measuring glucose
venous glucose
why is cap blood glucose not as useful
measured in whole capillary blood with poor precision tools that aren’t quality controlled
why is venous blood glucose gold standard
lab analysis with quality control
tube contains fluoride oxalate
causes of hypo without DM
fasting / reactive
paeds vs adult
critically unwell
organ failure - renal / liver
hyperinsulism
post gastric bypass
drugs
extreme weight loss
factitious
why does liver / kidnet failure give you hypos
liver - no stores of glycogen
kidney - no gluconeogenesis
what is the leading cause of hypos in people with DM
mismatch between carbs eaten and meds taken
other causes of hypos in DM
medications
inadequate carb intake / missed meal
impaired awareness of hypos
xs alcohol
strenuous exercise
AI conditions eg Addisons
what drugs other than insulin causes hypos
- sulphonylureas *
meglitinides (not used as much)
GLP 1 agonists with insulin
what non DM drugs increase risk of hypos
beta blockers
alcohol
what biochemical tests need to be done to determine cause of hypoglycaemia
insulin levels
c-peptide
drug screen
auto ABs
cortisol / GH
free fatty acids / blood ketones
lactate
when should biochemical tests be done to determine cause of hypo in non DM pts
only when they’re having the hypo !! useless if they’re not
what is C peptide
a marker of how much insulin the pancreas is making
what is the use of measuring C peptide and not just insulin
insulin reading tells you how much insulin is in the blood
C peptide tells you how much of that insulin was made by the pancreas - ie excludes exogenous insulin from injections
what are the 3 classifications of hypos based on insulin and C peptide
hypoinsulinaemic hypo (low insulin & CP)
hyperinsulinaemic hypo (high insulin & CP)
exogenous insulin (high insulin, low CP)
what does hypoinsulinaemic hypo indicate
normal response to a hypo - ie hypo is not caused by faulty insulin production
what does hyperinsulinaemic hypo indicate
hypo caused by too much insulin production
what does exogenous insulin hypo indicate
likely factitious insulin injection to intentionally cause hypo in non DM pt
(this is also seen in DM pts, but you wouldn’t bother measuring insulin & CP as you assume it is due to exogenous insulin already)
what causes of hypoglycaemia would have a hypoinsulinaemic hypo
all systemic causes
- starving / fasting
- exercise
- critically ill
- hypopituitarism / adrenal failure
- liver failure
- anorexia
what type of hypo do neonates have
hypoinsulinaemic hypo (normal)
why do neonates get hypoglycaemia
inadequate glycogen and fat stores
risk factors for neonatal hypoglycaemia
premature
co-morbidities
IUGR
SGA
inborn metabolic defects
give an example of an inborn metabolic defect that causes neonatal hypoglycaemia and the effect of this
fatty acid oxidation defect - no ketones produced but high fatty acids
causes of hyperinsulinaemic hypoglycaemia
islet cell tumour - insulinoma
drugs eg insulin, sulphonylureas
islet cell hyperplasia
rare genetic forms of hyperinsulism
rare AI
3 causes of islet cell hyperplasia
infant of diabetic mother
beckwith weidemann syndrome
nesidioblastosis
what is the commonest cause of hyperinsulinaemic hypoglycaemia
drugs
the others are super rare
Ix for hyperinsulinaemic hypoglycaemia due to ?insulinoma
glucose (low)
insulin (high)
c peptide (high)
sulphonylurea drug screen ( must be -‘ve to diagnose insulinoma)
describe how insulin is secreted in pancreas
glucose enters beta cell
undergoes glycolysis via glucokinase
ATP and glucose-6-P is produced
ATP closes the K+ channel
K+ prevented from leaving cell, so depolarises membrane
Ca2+ influx
Preformed insulin in vesicles fuse with membrane and are released
how do sulphonylureas work
they bind to the K+ channel (Sur 1 subunit) in beta islet cells and force it closed, irrespective of glucose level.
this causes membrane depolarisation and Ca influx which releases insulin from their vesicles
prevalance of insulinoma
1-2 million per year
when does hypoglycaemia occur in insulinoma
fasting only
what % of insulinomas are malignant? associated with MEN1?
10% malignant
8% associated with MEN1
Tx of insulinoma
resection
what is the rare cause of low glucose/insulin/CP/FFA AND ketones?
non islet cell tumour hypoglycaemia
eg secrete big IGF2 (an insulin like factor that mimicks insulin)
examples of non islet cell tumours causing hypos
mesenchymal tumours - mesotheliomas / fibroblastomas
epithelial carcinomas
who gets reactive / post prandial hypos
post gastric bypass surgery
hereditary fructose intolerance
early / pre DM
why do anorexics have hypos
poor glycogen stores in liver
