Diabetes and endo Flashcards
Dx T1DM
raised random BM >11.1
urine dip - glycosuira and ketones
fasting BM >7
Mx T1DM
Insulin therapy:
multiple daily injection basal bolus ( go to)- long acting insulin and short acting insulin before meals
continuous subcutaneous insulin infusion - programmable pump that delivers continuous supply
1, 2 or 3 insulin injections per day - short + long acting mixed together
HbA1C - at least 4 times per year, <48 (6.5%)
5 capillary BM per day (increased in times of stress - ie illness)
real time continuous glucose monitoring if:
frequent severe hypos
impairment of awareness of hypos (cause they faint)
can’t recognise or communicate symptoms of hypo
EXPLAIN HOW TO IDENTIFY DKA
monitor for complications from 12 years
causes of hypos
in neonates common as they have high energy requirements
insulin excess - overtreated, medication (SULPHONYLUREA), insulinoma, AI
w/o insulin excess: liver disease (glycogen stores), not eaten
reactive/non-fasting - galactosemia, maternal diabetes
mx of hypo
mild-moderate - oral glucose (lucozade), check BMs in 15 mins, as symptoms improve give long acting complex carbs
severe -
if in hospital give IV 10% glucose (5ml/kg bolus then steady)
if not in hospital - IM glucagon or conc glucose gel (seek help if no improvement in 10 mins)
causes of hypothyroidism
maldescent of thyroid
iodine deficiency
TSH deficiency
inborn hormone problems
How does congential hypothyroidism present
faltering growth feeding problems jaundice constipation pale skin hoarse cry
Mx hyperthyroidism
PTU or CBZ (causes neutropenia - safety net about going to doctors if sore throat or fever)
beta-blockers
2nd line - radio iodine or surgery
actions of PTH
Increase bone resorption
increase vit d metabolism to increase gut absorption
increase renal reabsorption of calcium
biochemistry of hypoparathyroidism
low calcium
low vit d
high posphate
normal ALP
cause of hypoparathyroidism
diGeorge - no thymus no parathyroid
biochemistry of pseudohypoparathyroidism
low calcium
high posphate
normal or elevated PTH
features of children with pseudohypoparathyroidism
short
fat
short metacarpals
teeth enamel hypoplasia
Mx of hypocalcaemia
acute - IV calcium glauconate
chronic - oral calcium, vit d analogues (avoid hypercalciuria as it can causes stones - monitor urine when on these)
Mx hypercalcaemia
rehydrate
diuretics (to remove excess Ca)
bisphosphonates
Presentation of CAH
virilisation of female
boys have large penis
develop secondary sexual characteristics early
salt losing (addisonian) crises
70-80% have failure of aldosterone production too (high potassium low sodium)
Dx CAH-
17ahydroxyprogesterone massively raised if salt losing: low sodium high potassium metabolic acidosis hypoglycaemia
Mx CAH
affected females can get surgery
acute salt losing crisis:
IV saline, IV hydrocortison, IV dextrose
Long term:
life long glucocorticoids to suppress ACTH (increase at times of stres)
MR if salt loss
monitor growth
Mx precocious puberty
gonadotrophin dependent:
GnRH agonist suppress puberty via negative feedbacl
GH therapy can stunt growth
gonadotrophin independent:
CAH - adjust aromatase inhibitors
McCune albright - ketoconzole, GnRH agonist, aromatase inhibitors
mx of delayed puberty
boys:
1 observation
2 3-6 months testosterone
girls:
1 observation
2 3-6 months oestrogen
causes of disorders of sexual development
excessive androgens in females (CAH)
inappropriate response to androgens in males:
can’t make DHT (aromatase deficiency), can’t respond to androgen (androgen insensitivity)
hermaphroditism - presence of XX and XY cells
If ambiguous genitalia measure sex hormons, adrenal hormones and karyotype
US internal structures
Mx DKA
When DKA diagnosed record -
vital signs, level of consciousness, dehydration status, body weight, hx of nausea or vom
measure -
pH + pCO2 (VBG), U+E, plasma bicarbonate
Fluid and insulin therapy
can give oral fluids and SC insulin if child is ALERT, not nauseous, vomiting or dehydrated
otherwise give IV
start IV insulin (0.05-0.1 units/kg/hr) infusion 1-2 hours after beginning IV fluid therapy in children
if no response after 6-8 hours increase insulin
IV fluid bolus:
shock - 20ml/kg saline
not shock - 10ml/kg
add this to maintenance fluids
consider catheter to monitor urine
How do you work out fluid deficit
5% fluid deficit in mild to mod DKA pH >7.1
10% fluid deficit in severe DKA pH <7.1
fluid deficit volume = % deficit x weight x 10
what are the maintenance fluid requirements in DKA
<10kg - 2ml/kg/hr
10-40 - 1ml/kg/hr
40+ - 40ml/hr
lower than usual because of risk of cerebral oedema
which fluids should you use in DKA
0.9% saline until glucose <14
0.9% saline + 5% glucose when glucose drops below 14
GIVE FLUIDS WITH 40MMOL/L KCL
When do you change from IV to SC insulin
Change when child is alert, not nauseous or vomiting, and can take oral fluids
Start SC insulin 30 minutes before IV finishes
Start pump 60 mins before IV finishes
monitoring in DKA
monitor BM, vital signs, fluid output, level of consciousness (mod. GCS) ever hour
NB - in children <2, severe DKA, or at high risk of cerebral oedema monitor GCS and HR every 30 mins
continuous ECG if on IV to check hypokalaemia (ST depression, flat p waves)
How to manage cerebral oedema in DKA
mannitol or hypertonic NaCl
How to manage hypokalaemia in DKA
<3mmol/L
stop infusion
discuss w/ paediatrc crit care consultant
what to discuss with DKA parents
factors that led to episode
how to manage intercurrent illness (viral illness)
arrange to see diabetes specialist
