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Year 4 Paediatrics > Paediatric Endocrinology > Flashcards

Paediatric Endocrinology Flashcards

1
Q

Investigations for T1DM

A

CBG
Urinary ketones
ABG - metabolic acidosis

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2
Q

Fasting blood glucose level

A

Positive = > 7mmol/l

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3
Q

Randome blood glucose level

A

Positive = > 11mmol/L

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4
Q

Ketoacidosis blood pH

A

pH < 7.3

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5
Q

Presentation of T1DM in children

A

May present with DKA

  • polydipsia
  • polyuria
  • fatigue and lethargy
  • weight loss

May have:

  • secondary enuresis
  • recurrent UTIs
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6
Q

Management of T1DM

A

Patient and family education

  • how ro take insulin subcut
  • how to monitor blood sugar
  • how to measure carb intake
  • how to monitor for complications

Insulin - long and short acting for a basal bolus regime

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7
Q

Insulin pump

A

Devices that continuously infuse insulin at different rates to control blood sugar levels

Cannula must be replaced every 2 - 3 days and the insertion site should be rotated

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8
Q

Who qualifies for an insulin pump

A

Over 12 yo

Difficulty controlling their HbA1c

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9
Q

Advantages and disadvantages of an insulin pump

A

Advantages:

  • less injections
  • less restrictions on diet
  • better blood control

Disadvantages:

  • difficult to use
  • needs to be worn at all times
  • may get blocked
  • small risk of infections
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10
Q

Types of insulin pump

A

Tethered pump - attached to belt that connects from the pump to the insertion site, controlled by the pump

Patch pump - sits directly on skin without tubes, when insulin runs out, the whole thing is replaced. Controlled by a remote

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11
Q

Causes of hypoglycaemia in diabetics

A 
Diarrhoea 
Vomiting 
Poor carbohydrate, insulin balance 
Infection - sepsis 
Malabsorption - coeliacs
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12
Q

Presentation of hypoglycaemia

A 
Hunger 
Fatigue 
Tremor 
Sweating 
Irritability 
Dizziness 
Pallor
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13
Q

Management of hypoglycaemia

A

Rapid acting glucose - lucozade
Slower acting carbs - biscuit

Severe:

  • IV fluids
  • IV dextrose 10%
  • IM glucagon
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14
Q

Pottasium during DKA

A

Can be high as lack of insulin to drive it into cells but less store

When treated with insulin, may get hypokalaemia which can lead to arrythmias

Therefore give pottasium via fluids

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15
Q

Complications of DKA

A

Cerebral oedema - dehydration and high blood sugar can move water into the extracellular space by osmosis, rapid correction of blood glucose can cause rapid water intake into brain cells causing oedema

Hypokalaemia/hyperkalaemia - arrythmias

Coma

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16
Q

Management of cerebral oedema

A

Slowing IV infusion of fluids
IV mannitol
IV hypertonic saline

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17
Q

Presentation of DKA

A 
Polyuria 
Polydipsia 
Fatigue
Nausea and vomiting 
Altered consciousness 
Acetone smell on breath 
Weight loss 
Dehydration
18
Q

Diagnostic criteria for DKA

A

Random CBG > 11mmol/l
Blood ketones > 3 mmol/l
Acidosis pH < 7.3

19
Q

Management of DKA

A
  1. IV fluids over 48 hours ( not too fast to prevent cerebral oedema)
  2. Fixed rate insulin infusion
  3. Once blood glucose falls < 14mmol/l give IV dextrose
20
Q

Addisons disease pathophysiology

A

Deficiency in cortisol or aldosterone due to a primary adrenal insufficiency

21
Q

Primary, secondary and tertiary adrenal insufficiency

A

Primary - adrenal glands do not produce enough cortisol or aldosterone

Secondary - lack of adrenal gland stimulation by ACTH commonly due to pituitary hypoplasia, surgery or infection

Tertiary - inadequate CRH release by the hypothalamus, often due to long term steroids ( 3+ weeks)

22
Q

Presentation of adrenal insufficiency

A

Babies:

  • vomiting and poor feeding
  • hypoglycaemia
  • jaundice
  • failure to thrive
  • lethargy

Children:

  • nausea and vomiting
  • poor weight gain or weight loss
  • reduced appetite
  • abdominal pain
  • muscle weakness or cramps
  • developmental delay
  • bronze hyperpigmentation
23
Q

Investigations for adrenal insufficiency

A 
Bloods - FBC, U+Es (hyperkalaemia) 
Blood glucose 
Synacthen test - ACTH 
Morning cortisol 
Aldosterone: renin ratio
24
Q

Addisons disease cortisol, renin, aldosterone and ACTH levels

A

Cortisol - low
Aldosterone - low
ACTH - high
Renin - high

25
Q

Secondary adrenal insufficiency cortisol, renin, aldosterone and ACTH levels

A

Cortisol - low
Aldosterone - normal
ACTH - low
Renin - normal

26
Q

Short synacthen test

A

ACTH stimulation test performed in the morning - synacthen is synthetic ACTH

Synacthen is given which should increase cortisol levels - cortisol measured at baseline and then 30 and 60mins after administration

Helps differentiate between primary and secondary adrenal insufficiency

27
Q

Management of adrenal insufficiency

A

IV Hydrocortisone - glucocorticoid which replaces cortisol
Fludrocortisone - mineralocorticoid which replaces aldosterone

Steroid card
Doses of ateroid increased during illness
Regular monitoring

28
Q

Monitoring for adrenal insufficiency

A 
Growth and devlopment 
Blood pressure 
U+Es 
Blood glucose
Bone profile 
Vitamin D
29
Q

Addisonian crisis presentation

A 
Reduced consciousness
Hypotension - dizziness 
Hypoglycaemia - loss of consciousness and fatigue 
Hyponatraemia - seizures 
Hyperkalaemia - arrythmias
30
Q

Cause of an Addisonian crisis

A

Abrupt cessation of steroids

First presentation of Addisons disease

31
Q

Management of a Addisonian crisis

A

IV fluids
IV hydrocortisone
IV fludrocortisone
Correct hypoglycaemia

32
Q

Pathophysiology of congenital adrenal hyperplasia

A

Congenital deficiency of the 21 hydroxylase enzyme which converts progesterone into cortisol and aldosterone causing an underproduction of cortisol and aldosterone and an overproduction of androgens

Autosomal recessive

33
Q

Presentation of congenital adrenal hyperplasia

A

Females - at birth can present with ambiguous genitalia and enlarged clitoris due to high testosterone

  • tall for age
  • facial hair
  • absent periods
  • deep voice
  • early puberty
  • Hyperpigmentation
  • Males - large penis, small testicles

Severe: hyponatraemia, hyperkalaemia and hypoglycaemia

  • poor feeding
  • vomiting
  • dehydration
  • arrythmias
34
Q

Management of congenital adrenal hyperplasia

A

Hydrocortisone - cortisol replacement
Fludrocortisone - aldosterone replacement
Females - may undergo surgery for ambiguous genitals

35
Q

Presentation of growth hormone deficiency

A

Neonates:

  • Micropenis
  • hypoglycaemia
  • severe jaundice

Infants:

  • poor growth
  • short stature
  • slow development of movement
  • delayed puberty
36
Q

Investigations for growth hormone deficiency

A

Growth hormone stimulation test - given glucagon or insulin (normally stimulates GH) and monitor levels of GH 2 - 4 hours after

Bloods - TFTs, cortisol, aldosterone, renin and ACTH
MRI brain - pituitary and hypothalamus
Genetic testing - Prader - Willi syndrome and Turners syndrome
Xray DEXA scan - bone age

37
Q

Treatment for growth hormone deficiency

A

Daily subcut injections of growth hormone - somatropin
Treatment of other hormone deficiencies
Close monitoring of height and development

38
Q

Presentation of congenital hypothyroidism

A 
Prolonged neonatal jaundice 
Poor feeding 
Constipation 
Increased sleeping 
Reduced activity 
Slow growth and development
39
Q

Conditions associated with hypothyroidism

A

Coeliacs disease

T1DM

40
Q

Common cause of aquired hypothyroidism

A

Hashimotos disease - due to anti- TPO antibodies (antithyroid peroxidase)

41
Q

Management of hypothyroidism

A

Levothyroxine orally ods

42
Q

Investigations for hypothyroidism

A

TFTs
Thyroid USS
Thyroid antibody tests

Year 4 Paediatrics (19 decks)

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