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hypoglycaemia Flashcards

1
Q

how would you manage acute hypoglycaemia in an alert and orientated patient ?

A
  1. Oral Carbohydrates:
    - Rapid acting; juice / sweets
    - Longer acting; sandwich

If Deteriorating: consider IM /SC 1mg Glucagon

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2
Q

how would you manage acute hypoglycaemia in a drowsy/confused patient ?

A

If swallow is intact;

  1. Buccal glucose
    - Hypostop / glucogel
    - > Consider IV access

Poor swallow OR unconscious;

  1. IV Access
    - 50 ml, 50 % glucose mini-jet
    - 100ml, 20% glucose

Deteriorating / refractory /insulin induced /difficult IV access: consider IM /SC 1mg Glucagon

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3
Q

patient has just had iv treatment for hypoglycaemia, they develop pain, redness, warmth and lump near the venous access site. whats happened?

A

extravasation of IV glucose: irritant, phlebitis

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4
Q

what 2 things should you remember about giving glucagon?

A
  1. mobilises glycogen stores so takes 15-20 mins to work

2. Danger of rebound hypoglycaemia, as will cause insulin release

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5
Q

What level of glucose defines hypoglycaemia?

A

numerous but generally less than 4

neonates is when it drops < 2.5 mmol/L (K meeran)

Neonate < 2 (according to NICU)

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6
Q

list some symptoms you may see in hypoglycaemia?

A

Adrenergic

  • tremor
  • sweating
  • palpitations
  • hunger

Neuro-glyco-paenic:

  • somnolence
  • confusion
  • seizures, coma
  • Incoordination

None

  • hypoglycaemic unawareness (lack of adrenergic symptoms during hypoglycaemia)
  • If a patient experiences recurrent hypoglycaemic episodes
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7
Q

what is the order of physiological change following the detection of hypoglycaemia?

A

○ Suppression of insulin
○ Release of glucagon
○ Release of adrenaline
○Release of acth, cortisol, gh

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8
Q

which hormones are involved in glucose counter-regulation?

A

The action of insulin is counterregulated by glucagon, adrenaline, noradrenaline, cortisol, and growth hormone.

These counterregulatory hormones constitute a principal defense against hypoglycemia, and levels are expected to rise as the glucose falls.

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9
Q

describe the events in glucose counter regulation

A

Low glucose -> A + B

A. Insulin suppressed + Glucagon increased:

- Reduce peripheral uptake of glucose
- Increase glycogenolysis
- Increase gluconeogenesis
- Increase lipolysis

Subsequently -> inc Glucose + FFA:
FFA -> beta oxidation -> ATP (energy) + ketones

B. low neuronal glucose sensed in hypothalamus

  • Sympathetic Activation - catecholamines
  • ACTH, cortisol and GH production
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10
Q

how does the hormone profile change in exercise-induced reduction in blood glucose ?

A

glucagon willl not be released as part of counter regulation, only;

adrenaline, noradrenaline, cortisol, and growth hormone.

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11
Q

how can you measure blood glucose ?

what is the gold standard?
which source of blood?
caveats?

A 
Lab Glucose:
Grey top (flouride oxalate)
Venous sample
2 mls blood
Gold std to make the diagnosis
Delay in results
Blood glucose meter
-Point-of-care device
-Instant result
- Capillary blood
But…
- Poor precision at low glucose levels
- Often poorly maintained
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12
Q

aetiology of hypoglycaemia in non-diabetic?

A 
Fasting or reactive?
Paediatric vs. adult
Critically unwell
Organ failure
Hyperinsulinism
Post gastric-bypass
Drugs
Extreme weight loss
Factitious
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13
Q

aetiology of hypoglycaemia in a diabetic patient?

A 
Diabetic Medications
Inadequate CHO intake / missed meal
Impaired awareness - due to to autonomic neuropathy
Excessive alcohol
Strenuous exercise

Co-existing autoimmune conditions - eg Addison’s- polyglandular autoimmune syndrome

Co-existing renal / liver failure alters drug clearance, and reduced doses needed.

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14
Q

which meds are associated with hypoglycaemia and why?

A

Oral Hypoglycaemic
Sulphonylureas e.g. glicazide
GLP-1 agents

Insulin
Rapid acting with meals: inadequate meal
Long-acting : hypo’s at night or in between meals

Other drugs
B-blockers, salicylates, alcohol ( inhibits lipolysis)

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15
Q

A very good HbA1c level in a diabetic, may be due to ?

A

reccurent hypos

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16
Q

impaired awareness of hypos may be due to __ ?

A

autonomic neuropathy

17
Q

how does continuous glucose monitoring work?

A

This device is applied to the abdominal wall with a small cannula that sits in the interstitial space in the subcutaneous fat

• The sensor does NOT accurately read blood sugar when it drops below 2.2 mmol/L
18
Q

How can we differentiate the cause of hypoglycaemia?

A

history, exam

take blood during hypos then;
biochemical tests; c-peptide, ketones, FFAs

19
Q

what is c peptide?

utility?

A

cleavage product of PRO insulin

C-peptide levels are a good marker of beta-cell function

Also good to help differentiate the cause of hypoglycaemia

20
Q

name some of the pharmacodynamics of insulin vs c-peptide?

A

Insulin:
Half-life, 4-6 minutes
Hepatic clearance
Exogenous insulin may interfere

C-peptide:
Half-life, ~ 30 minutes
Renal Clearance

21
Q

Hypoglycaemia due to excess injected insulin would result in what c-peptide level?

A

LOW c-peptide

because it comes from pro-insulin not insulin/ ready formed insulin

22
Q

patient presents with hypoglycaemia. what do the following results mean;

a. Low insulin, low C-peptide
b. High insulin, high C-peptide
c. High insulin, low C-peptide

which is the appropriate response to a hypo?

A

a. Hypoinsulinaemic hypoglycaemia
- appropriate response to a hypo
- not t1dm/dka as they would have hyperglycaemia

b. Hyperinsulinaemic hypoglycaemia - excess endogenous insulin production is causing the hypo
c. Exogenous insulin - injection

23
Q

What is 3-hydroxybutyrate?

A

a ketone body

aka beta-hydroxybutyrate

24
Q

What does the absence of ketones signify

(glucose 1.9, ketones negative)?

A

Fatty acid oxidation defect

25
Q

list some explainable and then pathological causes of neonatal hypoglycaemia

A 
Explainable
Maternal gestational diabetes
Premature, co-morbidities, IUGR, SGA
Inadequate glycogen and fat stores
Should improve with feeding

Pathological
Inborn metabolic defects eg:
- Fatty acid oxidation defect

26
Q

what is going on in the following picture and name some possible causes?

Neonatal hypoglycaemia with suppressed insulin + C-peptide.
FFA raised, but low ketones

A

suppressed insulin + C-peptide and rasied FFA is the appropriate response to hypoglycaemia BUT

there must be an error of metabolism of FFAs BECAUSE ketones must be raised as well

causes;
Inherited metabolic disorders: 
FAOD : no ketones produced 
GSD type 1 ( gluconeogenetic disorder)
Medium chain acyl coA dehydrogenase def.
Carnitine disorders

fatty acid oxidation defect
Glycogen Storage Disease

27
Q

name 3 ketone bodies?

A

Betahydroxybutyrate/ acetoacetate / acetone

28
Q

list some causes of the following presentation in a neonate:

persistent hypoglycaemia <2.5 (despite correction)
FFA normal/low
ketone normal/low

A

hyperinsulinism
(think logically: suppression of insulin normally leads to inc fatty acid production. so normal/low ffa must mean insulin is not suppressed)

hypopituitarism

29
Q

list some causes of the following presentation in a neonate:

persistent hypoglycaemia <2.5 (despite correction)
FFA raised
Ketone raised

A

Hepatomegaly:
haemochromatosis
gsd 1,3,6
fructose 1,6 phosphatase defi

No hepatomegaly:
GSD type 0
hereditary fructose intolerance
septicaemia
GH, corticosteroid deficiency and more
30
Q

list some causes of innapropriately high insulin levels?

A

Islet cell tumours – insulinoma
Drugs; insulin, sulphonylurea

Islet cell hyperplasia:
Infant of a diabetic mother
Beckwith Weidemann syndrome
Nesidioblastosis

31
Q

how would you screen for Sulphonylurea abuse?

A

Sulphonylurea drug screen – urine or serum

32
Q

what is the physiology of normal insulin secretion?

A

Glucose crosses the membrane and enters glycolysis via glucokinase
Glycolysis will produce ATP
The rise in ATP leads to closure of the ATP-sensitive K+ channel
The closure of this channel leads to membrane depolarisation, calcium influx and insulin exocytosis
NOTE: there are a lot of genetic mutations that affect this channe

33
Q

A Negative screen of what is required for diagnosing insulinoma?

why?

A

sulphonylurea

Sulphonylureas bind to the ATP-sensitive K+ channel and makes it close, independently of ATP

So, you get insulin release even when there is no ATP around - this is why sulphonylureas can cause hypoglycaemia

34
Q

charactersie and give the epidemiology of insulinomas.

hwo are they treated?

A

Usually small solitary adenoma
10% malignant
8% associated with MEN1

Treatment: resection

35
Q

whats is the diagnosis and reason behind:

Hypoglycaemia persists – glucose infusion
Insulin and C-peptide undetectable
Free fatty acids – undetectable
Ketones negative

A

Non-islet cell tumour hypoglycaemia

the secretion of big IGF-2
Big IGF-2 binds to IGF-1 receptors and insulin receptors
This behaves like insulin so your own endogenous insulin production is switched off and FFA production is suppressed

36
Q

list some genetic causes of hypoglycaemia with high insulin and c peptide

A

Glucokinase activating mutation

Congenital hyperinsulinism:
KCNJ11 /ABCC8
GLUD-1
HNF4A
HADH
37
Q

list causes for reactive/post-prandial hypoglycaemia?

A 
Hypoglycaemia following food intake
Can occur post-gastric bypass
Hereditary fructose intolerance
Early diabetes
In insulin sensitive  individuals after exercise or large meal

Path - chempath (25 decks)

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