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TAS Endocrinology > Hypoglycaemia ✅ > Flashcards

Hypoglycaemia ✅ Flashcards

1
Q

What history features should you pay attention to when evaluating a child with hypoglycaemia?

A
  • Autonomic symptoms
  • Neuroglycopenic symptoms
  • Pregnancy details (in neonate)
  • Relationship of symptoms to feeding
  • Access to oral hypoglycaemic medication
  • Family history of sudden infant death or consanguinity
  • Development of symptoms in response to certain foods
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2
Q

What are the autonomic symptoms of hypoglycaemia in a neonate?

A
  • Pallor
  • Sweating
  • Tachypnoea
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3
Q

What are the autonomic symptoms of hypoglycaemia in an older child?

A
  • Palpitations

- Tremor

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4
Q

What are the neuroglycopenic symptoms of hypoglycaemia in a neonate?

A
  • Jitteriness
  • Apnoea
  • Hypotonia
  • Feeding problems
  • Irritability
  • Abnormal cry
  • Convulsions
  • Coma
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5
Q

What are the neuroglycopenic symptoms of hypoglycaemia in older children?

A
  • Hunger
  • Abdominal pain
  • Nausea and vomiting
  • Pins and needles
  • Headache
  • Weakness
  • Dizziness
  • Blurred vision
  • Irritability
  • Mental confusion
  • Odd behaviour
  • Fainting
  • Convulsions
  • Coma
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6
Q

What pregnancy details should be considered when evaluating a neonate with hypoglycaemia?

A
  • Maternal symptoms of diabetes
  • Breech?
  • Birth weight
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7
Q

Why is it important to know if a neonate was breech in hypoglycaemia?

A

Breech said to be more common in hypopituitarism

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8
Q

Why is it important to know the birth weight of a neonate with hypoglycaemia?

A

Hypoglycaemia more common in IUGR or large for gestational age due to maternal diabetes

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9
Q

Why is it important to know the relationship of symptoms to hypoglycaemia?

A

Can help determine if due to inadequate fuel supply or excess fuel requirements, e.g. hyperinsulinism

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10
Q

Why is it important to know about access to oral hypoglycaemic medications?

A

May have been accidentally ingested

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11
Q

Why is it important to know about family history of SIDS or consanguinity?

A

Might suggest an inborn error of metabolism

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12
Q

What foods should you ask about symptom development in response to?

A

Foods containing lactose, fructose, or sucrose

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13
Q

What might symptom development in response to lactose, fructose, or sucrose suggest in hypoglycaemia?

A

Inborn errors in metabolism

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14
Q

What is usually found on examination in hypoglycaemia?

A

Most children with a history of hypoglycaemia will not have any abnormal clinical signs unless hypoglycaemic at the time

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15
Q

Why is it important to look for clinical signs on examination in hypoglycaemia?

A

May indicate associated diagnosis

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16
Q

What might suggest septo-optic dysplasia?

A

Optic atrophy

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17
Q

What is septo-optic dysplasia?

A

A rare congenital malformation syndrome featuring;

  • Underdevelopment of the optic nerve
  • Pituitary gland dysfunction
  • Absence of the septum pellucidum (a midline part of the brain)
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18
Q

What might suggest hypopituitarism?

A
  • Cranial midline defects
  • Short stature
  • Microgenitalia
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19
Q

What might suggest Addison’s disease?

A
  • Increased skin or buccal pigmentation

- Hypotension

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20
Q

What might suggest accelerated starvation?

A

Underweight or signs of malnutrition

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21
Q

What might suggest hyperinsulinism?

A
  • Tall stature

- Excess weight

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22
Q

What might suggest Beckwith-Wiedemann syndrome?

A
  • Abnormal ear lobe creases
  • Macroglossia
  • Umbilical hernia
  • Hemihypertrophy
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23
Q

What might suggest a glycogen storage disorder?

A

Hepatosplenomegaly

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24
Q

What is the aim of investigations in hypoglycaemia?

A
  • Establish severity

- Evaluate counter-regulatory responses and intermediary metabolite pathways

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25
Q

How is hypoglycaemia investigated?

A

Obtaining blood sample prior to treatment

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26
Q

What might be looked for on blood tests in hypoglycaemia?

A
  • Glucose
  • U&Es
  • Bicarb and pH
  • LFTs
  • Ammonia
  • Insulin and c-peptide
  • Cortical, ACTH, and growth hormone
  • Free fatty acids and beta-hydroxybutyrate
  • Acylcarnitine
  • Lactate
  • Alanine
27
Q

Why is glucose checked in hypoglycaemia?

A

Confirm severity

28
Q

Why are U&Es done in hypoglycaemia?

A

Look for evidence of adrenal insufficiency

29
Q

Why are bicarb and pH checked in hypoglycaemia?

A

Acidosis might imply adrenal failure or inborn error of metabolism

30
Q

Why should LFTs be done in hypoglycaemia?

A

May be abnormal in;

  • Primary liver disease
  • Sepsis
  • Glycogen storage disease
  • Galactosaemia
  • Fatty acid oxidation defects
  • Hereditary fructose intolerance
31
Q

What can ammonia show in hypoglycaemia?

A

Can be raised in a number of inborn errors of metabolism and some forms of hyperinsulinism

32
Q

What should happen to insulin and c-peptide in hypoglycaemia?

A

Should be suppressed

33
Q

What should happen to cortisol, ACTH, and GH in hypoglycaemia?

A

Should normally be elevated (implying appropriate stress response)

34
Q

What can free fatty acids and beta-hydroxybutyrate show in hypoglycaemia?

A

If elevated in proportion, imply lipolysis

35
Q

What can acylcarnitine show in hypoglycaemia?

A

Abnormal in some fatty acid oxidation defects

36
Q

What can lactate show in hypoglycaemia?

A

Elevated in;

  • Metabolic liver disease
  • Glycogen storage disorder
  • Sepsis
37
Q

What can alanine show in hypoglycaemia?

A

If low, suggests accelerated starvation

38
Q

What investigation should be done after glucose has been administered to correct the hypoglycaemia?

A

The next urine sample should be collected

39
Q

What testing is done on the urine sample in hypoglycaemia?

A
  • Screen for inborn errors of metabolism

- Toxicology screen

40
Q

What is looked for on a urine screen for inborn errors of metabolism?

A
  • Ketones
  • Reducing sugars
  • Dicarboxylic acids
  • Glycine conjugates
  • Carnitine derivatives
  • Amino acids
  • Organic acids
41
Q

What does the treatment of hypoglycaemia depend on?

A

Aetiology

42
Q

What can the causes of hypoglycaemia be broadly subdivided into?

A
  • Causes associated with reduced glucose availability due to detects in counter-regulatory responses (including limited supplies of glucose precursors)
  • Increased glucose consumption
43
Q

What causes of hypoglycaemia are due to reduced glucose availability?

A
  • IUGR
  • Prematurity
  • Hypopituitarism
  • Adrenal insufficiency
  • GH deficiency
  • Hypothyroidism
  • Accelerated starvation
  • Glucagon deficiency
  • Inborn errors of metabolism
  • Drugs
  • Liver dysfunction
  • Congenital heart disease
44
Q

What drugs can cause hypoglycaemia due to reduced glucose availability?

A
  • Alcohol
  • Aspirin
  • Beta blockers
45
Q

What does investigation of hypoglycaemia often find when the cause is reduced glucose availability?

A

Frequently fails to demonstrate any underlying abnormality

46
Q

When can accelerated starvation be diagnosed?

A

Only once other endocrine and metabolic causes are excluded

47
Q

What is accelerated starvation characterised by?

A

Normal endocrine counter-regulatory response with raised fatty acid and ketone responses

48
Q

What are the risk factors for accelerated starvation?

A
  • Boys

- Small for gestational age or thin physique

49
Q

What normally happens to accelerated starvation with time?

A

Usually resolves by puberty

50
Q

What does treatment of acceleration starvation involve?

A
  • Avoidance of prolonged fasting, particularly during illness
  • Administration of complex carbohydrates prior to bed
  • IV dextrose as required to reverse acute hypoglycaemia
51
Q

What are the causes of hypoglycaemia caused by increased glucose consumption?

A
  • Congenital hyperinsulinism
  • Transient neonatal hyperinsulinism
  • Infant to diabetic mother
  • Insulinoma
  • Beckwith-Wiedemann syndrome
  • Rhesus haemolytic disease
  • Perinatal asphyxia
  • Malaria
52
Q

What suggests hyperinsulinism?

A

Markedly excessive glucose requirements e.g. 12mg/kg/hour + to avoid hypoglycaemia

53
Q

What might congenital hyperinsulinism occur in relation to?

A

Several genetic defects affecting the regulation of insulin release

54
Q

What are the most commonly identified genetic defects in congenital hyperinsulinism?

A
  • ABCC8

- KCNJ11

55
Q

What does ABCC8 encode?

A

The sulphonylurea receptor

56
Q

What does KCNJ11 encode?

A

Potassium inward rectifying channel

57
Q

What are children affected by congenital hyperinsulinism at increased risk of?

A

Hypoglycaemia-induced brain damage

58
Q

Why are children with congenital hyperinsulinism at increased risk of hypoglycaemia-induced brain damage?

A

Hyperinsulinism suppresses not only glucose, but also ketone body production, which is an alternative cerebral fuel source

59
Q

What is the first line management for congenital hyperinsulinism?

A

Diazoxide and chlorothiazide treatment

60
Q

How does diazoxide evert its effects in congenital hyperinsulinism?

A

Through actions on the potassium channel, by;

  • Inducing hyperpolarisation
  • Decreasing calcium influx
  • Reducing insulin secretion
61
Q

What is second line management for congenital hyperinsulinism?

A

Somatostatin analogues

62
Q

How do somatostatin analogues work in congenital hyperinsulinism?

A

They exert a direct receptor-mediated inhibition of insulin release

63
Q

What are the surgical options for persistent cases of congenital hyperinsulinism?

A

Surgical excision of part of pancreas

64
Q

What has allowed for the technique of surgical excision of part of the pancreas in congenital hyperinsulinism?

A

Advances in understanding of genetics and new imaging techniques such as [18F]DOPA-PET scanning, which allows distinction between focal and diffuse pancreatic disease, with the former being curable by surgical excision with minimal morbidity

TAS Endocrinology (6 decks)

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