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TAS Endocrinology > Hyperglycaemia ✅ > Flashcards

Hyperglycaemia ✅ Flashcards

1
Q

What history is important in a child presenting with hyperglycaemia?

A
  • Duration of symptoms
  • Infection, particularly candidiasis
  • Vomiting or abdominal pain
  • Family history of diabetes or other autoimmune disease
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2
Q

What might vomiting and abdominal pain suggest with hyperglycaemia?

A

Ketoacidosis

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3
Q

What is often found on clinical examination in children with newly diagnosed diabetes?

A

No abnormal findings

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4
Q

What is critical in children with hyperglycaemia and presumed diabetes?

A

To distinguish between T1DM and T2DM

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5
Q

Why is it important to differentiate between T1DM and T2DM?

A

Treatment will be very different for each form

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6
Q

What suggests type 1 diabetes?

A
  • Weight loss
  • Dehydration
  • Signs of acidosis such as Kussmaul breathing
  • Sweet breath
  • Depressed consciousness
  • Signs of cerebral oedema
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7
Q

What is Kussmaul breathing?

A

Deep and tachypnoeic

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8
Q

What suggests type 2 diabetes?

A
  • Overweight
  • Hypertension
  • Acanthosis nigrans
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9
Q

What investigations need to be considered in hyperglycaemic children?

A
  • Glucose testing
  • HbA1c
  • GAD antibodies
  • Screening for other autoimmune disease
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10
Q

What are the forms of glucose testing?

A
  • Random
  • Two hour glucose tolerance test
  • Fasting
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11
Q

What is the diagnostic value for diabetes on random or GTT?

A

> 11.1mmol/L

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12
Q

What is the diagnostic value for diabetes on fasting blood glucose?

A

> 7mmol/L

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13
Q

What can HbA1c tell you in a newly presenting child with hyperglycaemia?

A

May indicate the length of the prodrome

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14
Q

What are GAD antibodies?

A

Glutamic acid decarboxylase antibodies

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15
Q

What does the presence of GAD antibodies suggest?

A

Autoimmune mediated T1DM

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16
Q

When is screening for other autoimmune diseases indicated?

A

When a diagnosis of T1DM seems likely

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17
Q

What testing can indicate T2DM when there is uncertainty?

A

Formal oral glucose tolerance test with measurement of high concentrations of insulin and c-peptide on baseline and 2 hour blood samples, along with suppressed sex hormone binding globulin concentrations

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18
Q

What is the most common form of childhood diabetes?

A

T1DM

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19
Q

What causes T1DM?

A

T-cell mediated autoimmune damage to pancreatic beta cells

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20
Q

What genes are implicated in T1DM?

A

Strong HLA associations with DQA, DQ8, and DRB

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21
Q

What kind of genes are DQA, DQ8, and DRB?

A

Major histocompatibility class II genes

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22
Q

How does the onset of T1DM compare between pre-school children and adolescents?

A

Has a more rapid onset in pre-school children

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23
Q

What does the rapidly increasing incidence of T1DM suggest?

A

An additional change in some unknown environmental precipitant, e.g. diet, viruses, hygiene, toxins

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24
Q

When do symptoms occur in T1DM, with regard to beta cells?

A

When approx 90% of beta cells are destroyed

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25
Q

What are children with T1DM at increased risk of?

A

Other autoimmune disease, e.g. coeliac, thyroid

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26
Q

What does treatment of T1DM require?

A

Insulin injections 2-4+ times a day, or delivered by pump in continuous subcutaneous injection

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27
Q

Give 2 examples of rapid acting insulins

A
  • Insulin lispro

- Insulin aspart

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28
Q

Why are insulin lispro and insulin aspart rapid acting?

A

Due to a change in their molecular structure, which prevents polymerisation into inactive hexamers following SC injection

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29
Q

Give 2 examples of long acting insulins

A
  • Insulin glargine

- Insulin detemir

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30
Q

Why is insulin glargine long acting?

A

Molecular changes shift it’s isoelectric point to result in precipitation and slow dissolution to release bioactive molecules

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31
Q

Why is insulin detemir long acting?

A

Molecular changes promote potent binding to albumin, which prolongs duration of active

32
Q

What is current research evaluating, regarding T1DM management?

A

Autoimmune modulation at diagnosis to prolong residual beta-cell activity

33
Q

What is required with any diagnosis of T1DM, with regards to support?

A

Considerable support and a detailed educational programme to help learn how to self manage diabetes

34
Q

What should be included in the education programme teaching how to self-manage T1DM?

A
  • Appropriate changes to insulin dose, guided by results of self blood glucose testing
  • Estimation of carbohydrate content of food
  • Estimation of known effects of exercise on their blood glucose measurements
35
Q

Why is optimal blood glucose control aimed for in T1DM?

A

Minimises microvascular complications

36
Q

How is blood glucose control judged in T1DM?

A

Repeated measurement of HbA1c (glycosylated haemoglobin)

37
Q

What causes glycosylated haemoglobin to rise?

A

It is a consequence of non-enzymatic glycation of haemoglobin when exposed to plasma glucose

38
Q

What causes glycosylated haemoglobin to rise?

A

It is a consequence of non-enzymatic glycation of haemoglobin when exposed to plasma glucose

39
Q

What does measuring HbA1c provide?

A

An integrated measure of circulating blood glucose over the previous 2-3 months

40
Q

When might HbA1c be unreliable?

A

In conditions which affect circulating red cell half life, e.g. haemoglobinopathies

41
Q

What is required for diabetes monitoring in conditions that affect circulating red cell half life?

A

Other measures such as continuous blood glucose monitoring or fructosamine

42
Q

What do patients and their carers need to be trained to do in T1DM, regarding hypoglycaemia?

A

Recognise and treat these episodes

43
Q

What does inadequate insulin lead to in the short term?

A

Hyperglycaemia

44
Q

What happens when hyperglycaemia exceeds the renal threshold for absorbing glucose?

A

Results in glycosuria and polyuria through concomitant osmotic effects

45
Q

What does excessive urinary loss of glucose lead to?

A

Negative calorie balance, and over time weight loss

46
Q

What does the cachexic state induced by chronic hyperglycaemia lead to in the long term?

A

Growth hormone resistance with impaired growth and suppressed gonadotrophin secretion, causing pubertal delay.

47
Q

How does excessive insulin deficiency lead to ketosis?

A

Due to lipolysis

48
Q

What does accumulation of ketones lead to?

A

Progressive acidosis with vomiting and impaired consciousness

49
Q

What does persistent hyperglycaemia produce in the longer term?

A

Microvascular changes

50
Q

What microvascular changes are caused by persistent hyperglycaemia?

A

The basement membrane of the epithelial cells becomes damaged through the presence of excess glycoproteins

51
Q

What do the microvascular changes in hyperglycaemia lead to?

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
52
Q

How does the presentation of T2DM compare to T1?

A

Similar, but ketoacidosis less common

53
Q

Are genetics involved in the development of T2DM?

A

There is a clear genetic predisposition, but different genes involved compared to T1

54
Q

What is the primary mechanism of development of T2DM?

A

Obesity-induced insulin resistance, with a secondary relative degree of insulin insufficiency, leading to excessive hepatic release of glucose

55
Q

What does the management of T2DM involve?

A

Lifestyle changes to increase physical activity and reduce calorie intake to promote weight loss and increase insulin sensitivity

56
Q

What do most children require in the management of T2DM?

A

Additional medical therapy using metformin

57
Q

How does metformin primarily act?

A

By suppressing hepatic gluconeogenesis

58
Q

What additional therapy (to metformin) may be required in the management of T2DM?

A
  • Sulphonylureas

- Insulin

59
Q

How do sulphonylureas act?

A

They bind to the potassium channel on the pancreatic beta cell, precipitating membrane depolarisation, calcium influx, and insulin release

60
Q

What screening is required in T2DM?

A

Screening for the development of microvascular complications

61
Q

What condition are teenage girls with T2DM at risk of?

A

PCOS

62
Q

What causes maturity onset diabetes of the young (MODY)?

A

Genetic defects of genes, mostly transcription factors, expressed in the beta-cell, producing variable defects in insulin secretion (but not action)

63
Q

What is MODY characterised by?

A

Mild asymptomatic hyperglycaemia in non-obese children

64
Q

What family history is MODY often characterised by?

A

Strong autosomal dominant family history of ‘diabetes’

65
Q

What is the risk of complications in MODY?

A

Low or non-existent

66
Q

Does MODY require treatment?

A

Most cases don’t

67
Q

What are some rare causes of diabetes mellitus?

A
  • Mutations in mitochondrial DNA

- Insulin sensitivity impaired by genetic defects in insulin receptor signalling

68
Q

Give 2 examples of conditions with mutations in mitochondrial DNA leading to diabetes

A
  • Maternally inherited diabetes and deafness syndrome

- Kearns-Sayre syndrome

69
Q

Give an example of a condition with genetic defecs in insulin receptor signalling

A

Leprechaunism

70
Q

Why are children with cystic fibrosis at increased risk of developing diabetes?

A

Combination of pancreatic destruction and insulin resistance, particularly during pulmonary exacerbations

71
Q

What treatment is requried with CF associated diabetes?

A

Insulin

72
Q

Why is insulin required with CF associated diabetes?

A

To support an unrestricted diet

73
Q

What care needs to be taken in CF associated diabetes?

A

To avoid hypoglycaemia

74
Q

Why is it particularly important to avoid hypoglycaemia in CF associated diabetes?

A

Due to increased risks associated with co-existent alpha cell damage

75
Q

What has neonatal diabetes recently been recognised to be due to?

A

Defects in genes expressed in the pancreatic beta cell

76
Q

What is the result of neonatal diabetes being due to defects in genes expressed in the pancreatic beta cell on the management?

A

Has shown that in those with mutations in certain genes (encoding the Kir6.2 subunit of the ATP-sensitive potassium channel KCNJ11), treatment with sulphonylureas can be even more effective than insulin, allowing patients to be weaned off daily injections

TAS Endocrinology (6 decks)

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