Hypoglycaemia Flashcards

1
Q

What is the acute management of hypoglycaemia in alert and oriented adults?

A

Oral Carbohydrates

Rapid acting; juice / sweets

Longer acting; sandwich

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2
Q

What is the acute management of hypoglycaemia in drowsy/ confused but in tact swallow adults?

A

Buccal glucose

e.g. Hypostop / glucogel

…start thinking about IV access

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3
Q

What is the acute management of hypoglycaemia in unconscious/ poor swallow adults?

A

IV access

50 ml, 50 % glucose mini-jet

Or 100 mls 20% glucose

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4
Q

What are caveats to acute treatment?

A

Treat, monitor, treat, monitor….
Beware extravasation of IV glucose: irritant, phlebitis
Glucagon mobilises glycogen stores so takes 15-20 mins to work
Are there glycogen stores to mobilise?
Danger of rebound hypoglycaemia, as will cause insulin release

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5
Q

What level of glucose defines hypoglycaemia?

A
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6
Q

How is glucose regulated?

A
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7
Q

Q1:What occurs first in response to hypoglycaemia?

A

Suppression of insulin

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8
Q

Investigations?

A

•Confirm there is hypoglycaemia

•Easy in a patient with diabetes

–usually monitor blood glucose (BG)

•Difficult in an otherwise healthy person

–May need to conduct a prolonged fast to demonstrate hypoglycaemia

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9
Q

Glucose measurment?

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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10
Q

Causes of hypoglycaemia?

A

Diabetics:

  • Commonest cause of hypoglycaemia
  • May be related to:

–Medications

–Inadequate CHO intake / missed meal

–Impaired awareness

–Excessive alcohol

–Strenuous exercise

–Co-existing autoimmune conditions

Non Diabetics:

Fasting or reactive?

Paediatric vs. adult

Critically unwell

Organ failure

Hyperinsulinism

Post gastric-bypass

Drugs

Extreme weight loss

Factitious

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11
Q

What are the diabetic medications?

A

•Oral Hypoglycaemic

–Sulphonylureas

–Meglitinides

–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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12
Q

How do co morbs affect hyoglycaemia?

A
  • Co-existing renal / liver failure alters drug clearance, and reduced doses needed.
  • Rarely concurrent Addison’s can result in hypos (polygladular autoimmune syndrome)
  • Caveats:
  • Poor awareness can occur due to autonomic neuropathy
  • Very serious problem at night, and an indication for continuous glucose monitoring
  • A very good HbA1c level in a diabetic, may be due to recurrent hypos.
  • End of the honeymoon period
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13
Q

How can we differentiate the cause of hypoglycaemia?

A
  • Thorough history and examination
  • Biochemical Tests

–Insulin levels

–C-peptide

–Drug screen

–Auto-antibodies

–Cortisol /GH

–Free fatty acids / blood ketones

–Lactate

–Other specialist tests – IGFBP/IGF-2/Carnitines etc.

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14
Q

What is C peptide?

A

It is the cleavage product of insulin

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

Also good to help differentiate the cause of hypoglycaemia

C peptide:

Half-life, ~ 30 minutes

Renal Clearance

Insulin:

Half-life, 4-6 minutes

Hepatic clearance

Exogenous insulin may interfere

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15
Q

Hypoglycaemia due to excess injected insulin would result in… (high/ low?) C peptide

A

low C peptide

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16
Q

20 year old female, BMI 17 kg/m2

Lanugo hair noted

Finger prick glucose – 3.8mmol/L

Routine bloods taken

•Doctor rung by lab 1 hr later as plasma glucose 2.6 mmol/L

What is the most likely cause of her low blood sugar?

A

poor glycogen liver storage

17
Q

What would the insulin and C-peptide result be if they had been measured in that patient?

A

unsure

18
Q

How does insulin/ c peptide change in different pathologies?

A
19
Q

Hypoglycaemia with low insulin + C-peptide?

A

Appropriate response to hypoglycaemia

Fasting / starvation

Strenuous exercise

Critical illness

Endocrine deficiencies

  • Hypopituitarism
  • Adrenal failure

Liver failure

Anorexia Nervosa

20
Q

What is 3-hydroxybutyrate?

A

A ketone body

21
Q

What does the absence of ketones signify (glucose 1.9, ketones negative)?

A

Fatty acid oxidation defect

22
Q

Neonatal Hypoglycaemia?

A

Explainable

  • Premature, co-morbidities, IUGR, SGA
  • Inadequate glycogen and fat stores
  • Should improve with feeding

Pathological

•Inborn metabolic defects

23
Q

Neonatal hypoglycaemia with suppressed insulin + C-peptide?

A
  • FFA raised, but low ketones
  • Inherited metabolic disorders

–FAOD : no ketones produced

–GSD type 1 ( gluconeogentic disorder)

–Medium chain acyl coA dehydrogenase def.

–Carnitine disorders

24
Q

Neonatal hypoglycaemia with suppressed insulin + C-peptide?

A

Expect high FFA

Expect detectable ketone bodies ( beta hydroxybutyrate, acetoacetate /acetone)

Good differentiators in neonatal hypoglycaemia

  • Insulin / C-peptide
  • FFA
  • KB
  • Lactate
  • Hepatomegaly
25
Q
A

read that again and write it out

26
Q

What causes inappropriate insulin levels?

A
  • Islet cell tumours – insulinoma
  • Drugs; insulin, sulphonylurea
  • Islet cell hyperplasia

–Infant of a diabetic mother

–Beckwith Weidemann syndrome

–Nesidioblastosis

27
Q

45 year old lady admitted fitting. Recurrently seen GP in previous months due to weight gain and increased appetite

Husband reports personality change in last few months.

Glucose 1.9 mmol/L

Insulin 35 mu/L

C-peptide 1000 pmol/L

What is the diagnosis?

A

Insulinoma or sulfonylurea excess

28
Q

Low glucose, high insulin and high C-peptide?

A

Low glucose, high insulin and high C-peptide

  • High C-peptide = endogenous insulin production
  • Insulinoma vs. Sulphonylurea abuse
  • Sulphonylurea drug screen – urine or serum
  • Negative sulphonylurea screen required for diagnosing insulinoma
29
Q

How do sulfonylureas work?

A

Sulfonylureas bind to and close ATP-sensitive K+ (KATP) (Sur1 subunit) channels on the cell membrane of pancreatic beta cells, which depolarizes the cell by preventing potassium from exiting. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granules with the cell membrane, and therefore increased secretion of mature insulin.

30
Q

What are Non-islet cell tumour hypoglycaemia?

A

•Non-islet cell tumour hypoglycaemia

–Tumours that cause a paraneoplastic syndrome

–Secretion of ‘big IGF-2’

–Big IGF2 binds to IGF-1 receptor and insulin receptor

–Mesenchymal tumours ( mesothelioma /fibroblastoma)

–Epithelial tumours ( carcinoma)

31
Q

What are insulinomas?

A

–1-2/million/year

–Usually small solitary adenoma

–10% malignant

–8% associated with MEN1

–Diagnosis, based on biochemistry + localisation

–Treatment: resection

32
Q

9 year old boy brought in fitting.

Glucose 1.9 mmol/L

Insulin 205 mu/L; C-peptide <33 pmol/L

What is the most likely cause of the low blood glucose?

A
  1. Glucose consumption during epileptic fit
  2. Stress response
  3. Factitious insulin
  4. Need more information
33
Q

What is factitous?

A

Factitious insulin / oral hypoglycaemic usage : always needs to be considered – more common than we think

Suspect in patients with access to insulin / drugs

34
Q

60 year old cachectic man found unconscious

Smoker

Glucose 1.9 mmol/L

Hypoglycaemia persists – glucose infusion

Insulin and C-peptide undetectable

Free fatty acids – undetectable

Ketones negative

The following diagnosis is likely

A

???

35
Q

What are the other causes of this picture:

↓ Glucose ↓ Insulin ↓ C-peptide

↓ FFA ↓ Ketones

A

Autoimmune conditions: rare

Antibodies to insulin receptors usually present with insulin resistance but rarely hypoglycaemia.

Autoimmune insulin syndrome

Ab’s directed to insulin, sudden dissociation may precipitate hypoglycaemia

Japan

Certain drugs : hydralazine, procainamide etc

36
Q

What are genetic causes of low glucose?

A

Glucokinase activating mutation

Congenital hyperinsulinism

  • KCNJ11 /ABCC8
  • GLUD-1
  • HNF4A
  • HADH
37
Q

What are reactive hypos?

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

–Difficult to define

38
Q
  • Type 1 diabetic 5 years
  • Previously well-controlled
  • Now recurrent hypos in morning

Hba1c 6.0 % Noted to be tired ++

Management?

A
  1. Review insulin dosing
  2. Review injection technique
  3. Consider pump therapy
  4. Perform a short synacthen test
  5. All of the above?