Paediatric Endocrinology Flashcards
Investigations for T1DM
CBG
Urinary ketones
ABG - metabolic acidosis
Fasting blood glucose level
Positive = > 7mmol/l
Randome blood glucose level
Positive = > 11mmol/L
Ketoacidosis blood pH
pH < 7.3
Presentation of T1DM in children
May present with DKA
- polydipsia
- polyuria
- fatigue and lethargy
- weight loss
May have:
- secondary enuresis
- recurrent UTIs
Management of T1DM
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
Insulin pump
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
Who qualifies for an insulin pump
Over 12 yo
Difficulty controlling their HbA1c
Advantages and disadvantages of an insulin pump
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
Types of insulin pump
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
Causes of hypoglycaemia in diabetics
Diarrhoea Vomiting Poor carbohydrate, insulin balance Infection - sepsis Malabsorption - coeliacs
Presentation of hypoglycaemia
Hunger Fatigue Tremor Sweating Irritability Dizziness Pallor
Management of hypoglycaemia
Rapid acting glucose - lucozade
Slower acting carbs - biscuit
Severe:
- IV fluids
- IV dextrose 10%
- IM glucagon
Pottasium during DKA
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
Complications of DKA
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
Management of cerebral oedema
Slowing IV infusion of fluids
IV mannitol
IV hypertonic saline
Presentation of DKA
Polyuria Polydipsia Fatigue Nausea and vomiting Altered consciousness Acetone smell on breath Weight loss Dehydration
Diagnostic criteria for DKA
Random CBG > 11mmol/l
Blood ketones > 3 mmol/l
Acidosis pH < 7.3
Management of DKA
- IV fluids over 48 hours ( not too fast to prevent cerebral oedema)
- Fixed rate insulin infusion
- Once blood glucose falls < 14mmol/l give IV dextrose
Addisons disease pathophysiology
Deficiency in cortisol or aldosterone due to a primary adrenal insufficiency
Primary, secondary and tertiary adrenal insufficiency
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)
Presentation of adrenal insufficiency
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
Investigations for adrenal insufficiency
Bloods - FBC, U+Es (hyperkalaemia) Blood glucose Synacthen test - ACTH Morning cortisol Aldosterone: renin ratio
Addisons disease cortisol, renin, aldosterone and ACTH levels
Cortisol - low
Aldosterone - low
ACTH - high
Renin - high
Secondary adrenal insufficiency cortisol, renin, aldosterone and ACTH levels
Cortisol - low
Aldosterone - normal
ACTH - low
Renin - normal
Short synacthen test
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
Management of adrenal insufficiency
IV Hydrocortisone - glucocorticoid which replaces cortisol
Fludrocortisone - mineralocorticoid which replaces aldosterone
Steroid card
Doses of ateroid increased during illness
Regular monitoring
Monitoring for adrenal insufficiency
Growth and devlopment Blood pressure U+Es Blood glucose Bone profile Vitamin D
Addisonian crisis presentation
Reduced consciousness Hypotension - dizziness Hypoglycaemia - loss of consciousness and fatigue Hyponatraemia - seizures Hyperkalaemia - arrythmias
Cause of an Addisonian crisis
Abrupt cessation of steroids
First presentation of Addisons disease
Management of a Addisonian crisis
IV fluids
IV hydrocortisone
IV fludrocortisone
Correct hypoglycaemia
Pathophysiology of congenital adrenal hyperplasia
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
Presentation of congenital adrenal hyperplasia
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
Management of congenital adrenal hyperplasia
Hydrocortisone - cortisol replacement
Fludrocortisone - aldosterone replacement
Females - may undergo surgery for ambiguous genitals
Presentation of growth hormone deficiency
Neonates:
- Micropenis
- hypoglycaemia
- severe jaundice
Infants:
- poor growth
- short stature
- slow development of movement
- delayed puberty
Investigations for growth hormone deficiency
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
Treatment for growth hormone deficiency
Daily subcut injections of growth hormone - somatropin
Treatment of other hormone deficiencies
Close monitoring of height and development
Presentation of congenital hypothyroidism
Prolonged neonatal jaundice Poor feeding Constipation Increased sleeping Reduced activity Slow growth and development
Conditions associated with hypothyroidism
Coeliacs disease
T1DM
Common cause of aquired hypothyroidism
Hashimotos disease - due to anti- TPO antibodies (antithyroid peroxidase)
Management of hypothyroidism
Levothyroxine orally ods
Investigations for hypothyroidism
TFTs
Thyroid USS
Thyroid antibody tests
