hypoglycaemia Flashcards

1
Q

acute mx of hypoglycaemia if pt alert and orientated

A

oral carbs
rapid acting - sweets/juice
longer acting - sandwich
deteriorating/refractory/insulin induced/difficult IV access - consider IM/SC glucagon

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2
Q

acute mx of hypoglycaemia if the patinet is drowsy/confused but swallow intact

A

buccal glucose
short acting - eg hypostop/glucogel
long acting - start thinking IV access
deteriorating/refractory/insulin induced/difficult IV access - consider IM/SC glucagon

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3
Q

acute mx of hyoglycaemia if unconscious or concerned about swallow

A

IV access
short acting - 20% glucose IV
long acting - 20% glucose
deteriorating/refractory/insulin induced/difficult IV access - consider IM/SC glucagon

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4
Q

caveats to consider when treating hypoglycaemia

A

need continuous monitoring
beware extravasation of IV glucose - irritant, phlebitis
glucagon mobilises glycogen stores - takes 15-20mins to work
need to check at 15-20 mins to see if the glucose has bumped up - and then check after this because reason for hypo might persist

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5
Q

what is the definition of hypoglycaemia

A

<4mmol/L - but sugar can regularly drop below this
abnormal when getting the sx of low blood sugar
however - can get impaired awareness
hypo when sx are relieved with glucose administration

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6
Q

sx of hypoglycaemia

A

first adrenergic
* tremor
* palpitations
* sweating
* hunger

then neuroglycopaenic
* somnolence
* confusion
* incoordination
* seizure
* coma

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7
Q

effect of low glucose on hormones

A

pancreas stop making insulin
increase glucagon
both lead to:
* reduce peripheral uptake of glcuose
* increased gluconeogenesis (from aa)
* increase glycogenolysis (liver)
* increase lipolysis (only if 0 insulin) -> increase in free atty acids -> beta oxidation -> increased ketone body

then low glucose sensed in hypothalamus -> SNS activation with catecholamines, then ACTH, cortisol, GH

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8
Q

first thing to when suspect hypoglycaemia

A

check actual hypo
easy to check when have dm - most will have glucometers

in healthy person - need to try to capture the hypo - bring into investigation unit - undertake prolonged fast for 72hr to precipitate hypo

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9
Q

glucose measurement

A

CBG - measured in whole blood, point of care, poor precision at low glucose level, not quality controlled

gold standard is venous glucose measyrement - collect in tube preserved with fluide oxalate, analysed in lab

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10
Q

causes of hypoglycaemia

A

fasting or reactive (ie bypass surgery)
paediatric vs adult
critically unwell
organ failure - liver = cant store glycogen // renal = where most gluconeogenesis occurs.
hyperinsulinism
drugs
extreme wht loss
factitious
diabetes

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11
Q

causes of hypos in diabetics q

A

meds - insulin and sulphonylureas (gliclazide)
inadequate carb intake/missed meal
impaired awareness
excessive alcohol
strenuous exercise and not reducing insulin
co-existing autoimmune eg Addison’s

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12
Q

meds that cause hypos

A

glucose lowering therapies
* sulphonylureas
* meglitinides
* glp-1 agents - only if given in conjunction with insulin because it boosts insulin production

insulin
* rapid acting with meals - inadequate meal
* long acting at night or in between meals

B blockers
salicyclates
alcohol - inhibits lipolysis

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13
Q

co-morbidities that can cause hypoglycaemia

A

renal/liver failure - alter drug clearance - dose reduction needed

addisons -> hypo

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14
Q

how can continuous glucose monitoring be helpful

A

see where the glucose level is flatlining - if stay at minimum readable value (2.2) for prolonged time - suggest impaired awareness

so have tech that stop them hypoing

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15
Q

how do we differentiate causes of hypoglycaemia outside of diabetes

A

hx and ex
ix - take bloods at time of hypo during 72hr fast
* insulin levels
* c peptide
* drug screen
* auto-Ab
* cortisol/GH
* FFA/blood ketones
* lactate
* special tests - IGFBP/IGF-2/Carnitines

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16
Q

summarise the structure of insulin

A

proinsulin is made of c-peptide and insulin
c-peptide levels are a good marker of beta cell function
insulin hlaf life 4-6 minutes
c-peptide half life 30mins

17
Q

classification of hypos using c peptide

A
hypoinsulinaemic hypoglycaemia is normal response to hypo
18
Q

causes of hypoinsulinaemic hypoglycaemia

A

fasting/starvation
strenuous exercise
critical illness
endocrine def - hypopit, adrenal failure
liver failure
anorexia nervosa

19
Q

causes of neonatal hypoglycaemia

A

explainable:
* premature, co-morbidities, IUGR, SGA
* inadequate glycogen and fat stores
* should improve with feeding

pathological
* inborn metabolic defects

20
Q

what happens with neonatal hypoglycaemia with suppressed insulin and c peptide

A

FFA raised but low ketones
can be due to inherited metabolic disorders:
* fatty acid oxidation defect: no ketones, high FFA, low insulin
* GSD type 1 (gluconeogentic disorder)
* medium chain acyl CoA dehydrogenase def
* carnitine disorders

fatty acid oxidation defect
21
Q

what is inappropriate hypoglycaemia and causes

A

when glucose is low due to high insulin

islet cell tumours - insulinoma
drugs - insulin, sulphonylurea
islet cell hyperplasia - infant of diabetic mother, beckback weidemann syndrome, nesidioblastosis
rare genetic forms
autoimmune

21
Q

what is inappropriate hypoglycaemia and causes

A

when glucose is low due to high insulin

islet cell tumours - insulinoma
drugs - insulin, sulphonylurea
islet cell hyperplasia - infant of diabetic mother, beckback weidemann syndrome, nesidioblastosis
rare genetic forms
autoimmune

22
Q

what is dx - low glucose, high insulin and c peptide

A

means insulin is endogenous - so ddx: insulinoma vs sulphonylurea abuse
drug screen - urine/serum
-ve sulphonylurea screen is needed to dx insulinoma

23
Q

summarise normal insulin secretion and how do sulphonylureas work

A

Glucose into B cecll - > glycolysis -> atp
K channel close
Membrane depol
Ca comes in
Insulin granules fuse with membrane and release insulin
Sulphonylurea bind to K+ATP channel -> closes independently of glucose - get release of insulin

24
summarise insulinoma
rare solitary adenoma 10% malignant, 8% associated with MEN1 usually fasting hypos dx - based on biochem (low glucose, high insulin and c peptide) and localisation Rx - resection
25
summarise non-islet cell tumour hypoglycaemia
tumours that cause a paraneoplastic syndrome secretion of 'big IGF-2' big IGF-2 binds to IGF-1 receptor and insulin receptor - ie doing the job of insulin mesenchymla tumours - mesothelioma/fibroblastoma epithelial tumours - carcinoma low insulin, low c peptide, if FFA and ketones are low -> non-islet cell tumour hypoglycaemia
25
summarise non-islet cell tumour hypoglycaemia
tumours that cause a paraneoplastic syndrome secretion of 'big IGF-2' big IGF-2 binds to IGF-1 receptor and insulin receptor - ie doing the job of insulin mesenchymla tumours - mesothelioma/fibroblastoma epithelial tumours - carcinoma low insulin, low c peptide, if FFA and ketones are low -> non-islet cell tumour hypoglycaemia
26
autoimmune cause of hypoglycaemia
Ab to insulin receptors -> insulin resistance but rarely hypo autoimmune insulin syndrome - Abs directed to insulin, sudden dissociation may -> hypo high incidence in japan associated with hydralazine, procainamide
27
genetic cause of hyperinsulinism
glucokinase activating mutation congenital hyperinsulinism * KCNJ11/ABCC8 * GLUD-1 * HNF4A * HADH really hard to treat low glucose, high insulin and c peptide
28
reactive postprandial causes of hypoglycaemia
post food intake can happen after gastric bypass hereditory fructose intolerance early dm in insulin sensitive people after exercise or large meal true post-prandial - difficult to define