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Year 4 - Paediatrics > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Outline the homeostatic mechanism behind control of elevated blood glucose.

A

Insulin is produced by beta cells in the Islets of Langerhans in the pancreas, causing a reduction in blood sugar.

It causes cells to:

  1. Absorb glucose from the blood and use it as energy (glucolysis)
  2. Store glucose as glycogen in the liver and muscle cells (glycogenesis).
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2
Q

Outline the homeostatic mechanism behind control of decreased blood glucose.

A

Glucagon is produced by alpha cells in the Islets of Langerhans in the pancreas, causing a rise in blood glucose.

It causes the liver to:

  1. Break down stored glycogen into glucose (glycogenolysis).
  2. Convert fats and proteins into glucose (gluconeogenesis).
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3
Q

Outline the mechanism behind ketogenesis.

A

In prolonged fasting, there is insufficient supply of glucose and glycogen stores are exhausted.

The liver takes fatty acids and converts them to ketones, which can be used as fuel.

Ketones can dissociate into a conjugate acid and base, causing an acidosis.

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4
Q

What is Type 1 diabetes mellitus (T1DM)?

A

An autoimmune disease where the alpha cells in the Islets of Langerhangs in the pancreas are targeted, reducing the capacity to produce insulin.

This means cells cannot take up glucose, so the level of glucose in the blood rises to cause hyperglycaemia.

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5
Q

Presentation of Type 1 diabetes mellitus.

A

Triad of hyperglycaemia:
- polyuria
- polydispsia
- weight loss

DKA is the presentation in up to 50% of new diagnoses.

Other less typical presentations include secondary enuresis and recurrent infections.

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6
Q

T1DM aetiology.

A
  • autoimmune
  • genetic
  • infective trigger
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7
Q

When a new diagnosis of T1DM, what additional bloods should be considered?

A

Baseline bloods including FBC, U&E and laboratory glucose.

Blood cultures if suspected infection (i.e. fever).

HbA1c

TFTs and TPO to test for associated autoimmune thyroid disease.

anti-TTG and serum IgA to test for associated coeliac disease.

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8
Q

Which antibodies are associated with T1DM?

A
  • insulin antibodies
  • anti-GAD antibodies
  • islet cell antibodies
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9
Q

General management of T1DM.

A

Manage via a multidisciplinary team:
- s/c insulin regimes
- dietary carbohydrate intake monitoring
- monitor blood sugar levels on waking, at each meal and before bed
- monitor for and manage complications

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10
Q

Usual insulin prescription in T1DM.

A

Basal Bolus regime.

Basal refers to an injection of a long acting insulin, typically in the evening.

Bolus refers to an injection of a short acting insulin, typically three times a day before meals.

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11
Q

When is an insulin pump considered in the management of T1DM?

A
  • age >12 years
  • difficulty controlling HbA1c
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12
Q

Advantages of insulin pumps.

A
  • better blood sugar control
  • more flexibility with eating
  • less injections
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13
Q

Disadvantages of insulin pumps.

A
  • difficulty learning to use the pump
  • attached all the time
  • blockages in the infusion set
  • risk of infection
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14
Q

What are the short term complications of T1DM?

A
  • hypoglycaemia
  • hyperglycaemia
  • DKA
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15
Q

Symptoms of hypoglycaemia.

A
  • hunger
  • tremor
  • sweating
  • irritability
  • dizziness
  • pallor

Severe hypoglycaemia will lead to reduced consciousness, coma and death.

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16
Q

Treatment of hypoglycaemia.

A

A combination of rapid acting glucose (e.g. lucozade) and slower acting carbohydrates (e.g. biscuits, toast).

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17
Q

Treatment of severe hypoglycaemia.

A

IV 10% dextrose if a cannula is in situ.

Otherwise IM glucagon.

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18
Q

Causes of hypoglycaemia.

A
  • insulin overdose
  • carbohydrate malabsorption (e.g. vomiting, diarrhoea)
  • hypothyroidism
  • growth hormone deficiency
  • liver cirrhosis
  • alcohol
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19
Q

Treatment of hyperglycaemia.

A

Increase the insulin dose.

It can take several hours to take effect and repeated doses could lead to hypoglycaemia.

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20
Q

Triad of DKA.

A
  • acidosis (pH <7.3; bicarbonate <15mmol/L)
  • ketonaemia
  • blood glucose >11mmol/L
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21
Q

What are the three key complications of DKA that lead to death?

A
  1. Cerebral oedema
  2. Hypokalaemia
  3. Aspiration pneumonia
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22
Q

Pathophysiology of DKA.

A

Absolute deficiency of insulin in T1DM leads to a rise in glucagon.

Under the action of glucagon, the rate of gluconeogenesis and lipolysis increased. The catabolism of adipose tissue results in rising levels of acidic ketone bodies.

The hyperglycaemia and glycosuria causes osmotic diuresis, resulting in dehydration.

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23
Q

Risk factors for DKA.

A

Lack of insulin:
- non-compliance with insulin treatment
- device failure
- changing insulin requirements during puberty

An excess of glucose:
- increased ingestion of glucose

Intercurrent illness (ie. infection)

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24
Q

Symptoms of DKA.

A
  • lethargy
  • N+V
  • abdominal pain

Background hx of T1DM symptoms or diagnosis:
- weight loss
- polyuria
- polydipsia

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25
Q

Signs of DKA.

A
  • tachypnoea
  • subcostal and intercostal recession
  • tachycardia
  • hypotension
  • dry mucous membranes
  • abdominal pain
  • reduced consciousness
  • ketonic breath

NB: Fever is NOT a feature of DKA. If present, suspect an underlying infection.

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26
Q

Differentials to DKA.

A
  • hyperosmolar hyperglycaemic state
  • new presentation of T1DM.
  • dehydration
  • sepsis
  • appendicitis
  • intussusception
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27
Q

Diagnostic workup for DKA.

A
  • bedside blood glucose and ketones
  • capillary blood gas
  • laboratory blood glucose, U&Es*, FBC and creatinine
  • 12 lead ECG*

*monitoring for signs of hyper- or hypokalaemia

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28
Q

Emergency treatment of DKA.

A
  • 100% oxygen NRM
  • fluid bolus
  • NG tube if vomiting
  • delayed IV insulin (1-2 hours)
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29
Q

Presentation of cerebral oedema.

A
  • headache
  • confusion
  • irritability
  • increased droswiness
  • hypertension with bradycardia
  • focal neurological signs
  • papilloedema
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30
Q

Prognosis of DKA.

A

Majority of children who present in DKA will recover well and be discharged from home within a few days.

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31
Q

Macrovascular complications of T1DM.

A
  • coronary artery disease
  • peripheral ischaemia
  • stroke
  • hypertension
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32
Q

Microvascular complications of T1DM.

A
  • peripheral neuropathy
  • retinopathy
  • glomerulosclerosis
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33
Q

Infection related complications of T1DM.

A
  • UTIs
  • pneumonia
  • skin and soft tissue infection
  • fungal infections (e.g. oral and vaginal candidiasis)
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34
Q

T1DM monitoring.

A

HbA1c every 3 to 6 months to track the average blood sugar over time.

Capillary blood glucose allows for self-monitoring and adjustments in insulin dose.

Flash glucose (e.g. Libre) monitoring measures the glucose level in the subcutaneous tissue. There is a 5 minute lag behind blood glucose.

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35
Q

What is the cause of cerebral oedema in DKA?

A

Dehydration causes increased blood sugar concentration, decreasing osmolality.

Water moves down its water potential gradient from the intracellular space in the brain, to the extracellular space.

this causes the brain to swell and become oedematous.

36
Q

What is adrenal insufficiency?

A

Where the adrenal glands do not produce enough steroid hormones, particularly cortisol and aldosterone.

37
Q

What is Addison’s disease?

A

Primary adrenal insufficiency, where autoimmune damage to the adrenal glands results in a reduced secretion of cortisol and aldosterone.

38
Q

Causes of secondary adrenal insufficiency.

A

Inadequate ACTH to release the adrenal glands, resulting in low levels of cortisol being released.

This is the result of loss or damage to the pituitary gland:
- congenital hypoplasia
- surgery
- infection
- loss of blood flow
- radiotherapy

39
Q

Causes of tertiary adrenal insufficiency.

A

Inadequate CRH release by the hypothalamus causes suppression of the hypothalamus.

This is usually the result of patients being on long term oral steroids. When the exogenous steroids are suddenly withdrawn, the hypothalamus cannot produce endogenous steroids adequately.

Therefore, long term steroids should be tapered slowly to allow time for the adrenal axis to regain normal function.

40
Q

Features of adrenal insufficiency in babies.

A
  • lethargy
  • vomiting
  • poor feeding
  • hypoglycaemia
  • jaundice
  • failure to thrive
41
Q

Features of adrenal insufficiency in older children.

A
  • N+V
  • poor weight gain or weight loss
  • reduced appetite
  • abdominal pain
  • muscle weakness or cramps
  • developmental delay
  • bronze hyperpigmentation
42
Q

Physiology behind bronze hyperpigmentation in Addison’s.

A

Primary adrenal insufficiency causes the pituitary to compensate by producing more ACTH.

ACTH stimulates melanocytes, so there is more melanin (i.e. pigment) produced.

43
Q

Diagnostic workup for adrenal insufficiency.

A

Main bloods:
- cortisol
- ACTH
- aldosterone
- renin

Check U&Es for hyponatraemia and hyperkalaemia, and blood glucose for hypoglycaemia.

44
Q

Blood results consistent with Addison’s disease.

A

Cortisol - low

ACTH - raised

Aldosterone - low

Renin - raised

45
Q

Blood results consistent with secondary adrenal insufficiency.

A

Cortisol - low

ACTH - low

Aldosterone - normal

Renin - normal

46
Q

Outline the use of the ACTH stimulation test.

A

Used to confirm adrenal insufficiency.

  1. Administer synacthen
  2. Measure blood cortisol at baseline, 30 and 60 minutes after administration

The cortisol level should at least double in response to synacthen; a failure of cortisol to rise indicates primary adrenal insufficiency.

47
Q

Ongoing management of adrenal insufficiency in children.

A

Maintenance dosage of steroids (hyrocortisone and fludrocortisone).

Monitoring via MDT:
- growth and development
- blood pressure
- U&Es
- glucose
- bone profile
- vitamin D

48
Q

Sick day rules when taking steroids.

A

Individualised care plan documenting how to manage acute illness:
- double dose of steroid while ill
- monitor blood glucose closely

With diarrhoea and vomiting, they need an IM injection of steroid at home, and may require admission for IV steroids.

49
Q

What is adrenal crisis?

A

The acute presentation of severe Addison’s, with a life-threatening absence of steroid hormones.

50
Q

Presentation of adrenal crisis.

A
  • reduced consciousness
  • hypotension
  • hypoglycaemia
  • hyponatraemia
  • hyperkalaemia
51
Q

Causes of adrenal crisis.

A
  • first presentation of Addison’s disease
  • infective trigger
  • trauma trigger
52
Q

Management of adrenal crisis.

A
  • intensive monitoring
  • IV hydrocortisone
  • IV fluid resuscitation
  • correct hypoglycaemia
  • careful monitoring of electrolytes and fluid balance
53
Q

Inheritance pattern of congenital adrenal hyperplasia.

A

Autosomal recessive pattern causing congenital deficiency of 21-hydroxylase enzyme.

54
Q

Normal function of 21-hydroxylase enzyme.

A

Progesterone&raquo_space; aldosterone + cortisol

55
Q

Pathophysiology of congenital adrenal hyperplasia.

A

An inherited deficiency in 21-hydroxylase means progesterone cannot be converted to aldosterone and cortisol.

This causes an increase in serum progesterone, some of which is converted to testosterone instead.

This results in a patient with:
- low aldosterone
- low cortisol
- high testosterone

56
Q

Presentation of severe CAH.

A
  • females have ambiguous genitalia at birth
  • hyponatraemia
  • hyperkalaemia
  • hypogylcaemia

Results in the following signs and symptoms:
- poor feeding
- vomiting
- dehydration
- arrhythmias

57
Q

Presentation of mild CAH in females.

A

Due to high androgen levels:
- tall for age
- facial hair
- absent periods
- deep voice
- early puberty

58
Q

Presentation of mild CAH in males.

A

Due to high androgen levels:
- tall for age
- deep voice
- large penis
- small testicles
- early puberty

59
Q

Why is skin hyperpigmentation a feature of CAH?

A

The anterior pituitary gland responds to the low levels of cortisol by producing increasing amounts of ACTH.

ACTH stimulates melanocytes, increasing the production of melanin.

60
Q

Management of CAH.

A

Coordinated by specialist paediatric endocrinologists:
- cortisol replacement with hydrocortisone
- aldosterone replacement with fludrocortisone
- female patients with ambiguous genitalia may require corrective surgery

61
Q

What is the function of growth hormone?

A

Stimulating cell reproduction and the growth of organs, muscles, bones and height.

62
Q

Pathophysiology of congenital growth hormone deficiency.

A

A disruption to the growth hormone axis at the hypothalamus or pituitary gland.

Due to a genetic mutation:
- GH1 deficiency
- GHRHR defect

63
Q

Presentation of growth hormone deficiency in neonates.

A
  • micropenis (males)
  • hypoglycaemia
  • severe jaundice
64
Q

Presentation of growth hormone deficiency in infants and children.

A
  • poor growth (stopping or slowing at age 2-3)
  • short stature
  • slow development of movement and strength
  • delayed puberty
65
Q

How is growth hormone deficiency investigated?

A

Growth hormone stimulation test.

Administer glucagon or insulin, and monitor growth hormone levels regularly for 4 hours.

In growth hormone deficiency, there will be a poor response to stimulation.

66
Q

Diagnostic workup for growth hormone deficiency.

A
  • growth hormone stimulation test
  • TFTs (?hypothyroidism)
  • cortisol, ACTH, renin, aldosterone (?adrenal deficiency)
  • MRI brain (?structural abnormalities to pituitary gland / hypothalamus)
  • genetic testing (?Turner syndrome / Prader-Willi syndrome)
  • wrist xray to determine bone age and predict final height
67
Q

Treatment of growth hormone deficiency.

A

Paediatric endocrinologist involvement:
- s/c injections of growth hormone
- treatment of associated hormone deficiencies
- close monitoring of height and pubertal development

68
Q

Pathophysiology of congenital hypothyroidism.

A

A child is born with an underactive thyroid gland, caused by:
- underdeveloped thyroid gland
- under-secreting thyroid gland

69
Q

Presentation of congenital hypothyroidism.

A

Screened for on the newborn blood spot screening test.

Where it is not picked up at birth, patients can present with:
- prolonged neonatal jaundice
- poor feeding
- constipation
- increased sleeping
- reduced activity
- slow growth and development

70
Q

Pathophysiology of acquired hypothyroidism.

A

The most common cause of acquired hypothyroidism is Hashimoto’s thyroiditis.

This causes autoimmune inflammation of the thyroid gland and subsequent under activity of the gland.

71
Q

Which antibodies are associated with Hashimoto’s thyroiditis?

A

Anti-TPO and anti-Tg antibodies.

72
Q

Presentation of acquired hypothyroidism.

A
  • fatigue and low energy
  • poor growth
  • weight gain
  • poor school performance
  • constipation
  • dry skin and hair loss
73
Q

Investigations of hypothyroidism.

A
  • TFTs
  • thyroid ultrasound
  • thyroid antibodies (anti-TPO and anti-Tg)
74
Q

Management of hypothyroidism in children.

A

Levothyroxine.

Dose is titrated based on TFTs and symptoms.

75
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease - autoimmune activation of the thyroid gland by TSH receptor antibodies, producing excessive thyroid hormone.

76
Q

Other causes of hyperthyroidism.

A
  • toxic multinodular goitre
  • toxic adenoma
  • thyroid carcinoma
  • neonatal hyperthyroidism
77
Q

Risk factors for hyperthyroidism.

A
  • FHx of thyroid disease
  • FHx of autoimmune disease
  • increased iodine intake
  • smoking
  • female
78
Q

Clinical features of hyperthyroidism.

A
  • weight loss / failure to thrive
  • increased appetite
  • rapid growth in height
  • sweating
  • heat intolerance
  • fatigue
  • anxiety
  • diarrhoea
  • palpitations
  • psychosis
  • oligo- / amenorrhoea
79
Q

Signs of hyperthyroidism.

A
  • goitre (move on swallowing)
  • fine tremor
  • hyperreflexia
  • moist, warm skin
  • tachycardia
  • proximal muscle wasting
  • hair loss
80
Q

Diagnostic workup for hyperthyroidism.

A
  • TFTs
  • TPO and TSH receptor antibodies
  • USS thyroid
81
Q

Management of Grave’s disease.

A

Carbimazole titrated to TFT levels and symptoms.

A block and replace regime can be used (carbimazole + levothyroxine).

For symptom relief, propanolol can be given for the first few weeks.

NICE recommends titrating carbimazole for 2 years, then stopping the drug to see if they have gone into remission.

82
Q

Side effects of carbimazole.

A
  • rashes
  • nausea
  • headaches
  • agranulocytosis
  • hepatitis
  • autoimmune pancreatitis
83
Q

Presentation of thyroid storm.

A
  • fever
  • hyperthermia
  • tachycardia
  • hypertension
  • GI dysfunction
  • CNS dysfunction
  • seizures
84
Q

Treatment of thyroid storm.

A
  • IV fluids
  • large dose of propylthiouracil
  • propranolol
  • hydrocortisone
85
Q

Complications of untreated hyperthyroidism.

A
  • weight loss
  • hypercalcaemia
  • osteoporosis and fragility fractures
  • cardiovascular dysfunction
  • embolic events
86
Q

What is neonatal hyperthyroidism?

A

Mother has Grave’s disease.

Even in remission, TSH receptor antibodies can cross the placenta and cause hyperthyroidism in neonates.

Usually self-limiting and resolves spontaneously within 1-3 months.

Year 4 - Paediatrics (17 decks)

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