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PATHOLOGY > hypoglycaemia > Flashcards

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
Q

summarise insulinoma

A

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
Q

summarise non-islet cell tumour hypoglycaemia

A

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
Q

summarise non-islet cell tumour hypoglycaemia

A

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
Q

autoimmune cause of hypoglycaemia

A

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
Q

genetic cause of hyperinsulinism

A

glucokinase activating mutation
congenital hyperinsulinism
* KCNJ11/ABCC8
* GLUD-1
* HNF4A
* HADH

really hard to treat
low glucose, high insulin and c peptide

28
Q

reactive postprandial causes of hypoglycaemia

A

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

PATHOLOGY (94 decks)

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