Diabetes and endo Flashcards

1
Q

Dx T1DM

A

raised random BM >11.1
urine dip - glycosuira and ketones
fasting BM >7

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2
Q

Mx T1DM

A

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

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3
Q

causes of hypos

A

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

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4
Q

mx of hypo

A

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)

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5
Q

causes of hypothyroidism

A

maldescent of thyroid
iodine deficiency
TSH deficiency
inborn hormone problems

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6
Q

How does congential hypothyroidism present

A
faltering growth
feeding problems
jaundice
constipation
pale skin 
hoarse cry
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7
Q

Mx hyperthyroidism

A

PTU or CBZ (causes neutropenia - safety net about going to doctors if sore throat or fever)
beta-blockers
2nd line - radio iodine or surgery

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8
Q

actions of PTH

A

Increase bone resorption
increase vit d metabolism to increase gut absorption
increase renal reabsorption of calcium

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9
Q

biochemistry of hypoparathyroidism

A

low calcium
low vit d
high posphate
normal ALP

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10
Q

cause of hypoparathyroidism

A

diGeorge - no thymus no parathyroid

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11
Q

biochemistry of pseudohypoparathyroidism

A

low calcium
high posphate
normal or elevated PTH

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12
Q

features of children with pseudohypoparathyroidism

A

short
fat
short metacarpals
teeth enamel hypoplasia

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13
Q

Mx of hypocalcaemia

A

acute - IV calcium glauconate

chronic - oral calcium, vit d analogues (avoid hypercalciuria as it can causes stones - monitor urine when on these)

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14
Q

Mx hypercalcaemia

A

rehydrate
diuretics (to remove excess Ca)
bisphosphonates

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15
Q

Presentation of CAH

A

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)

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16
Q

Dx CAH-

A
17ahydroxyprogesterone massively raised 
if salt losing:
low sodium
high potassium
metabolic acidosis
hypoglycaemia
17
Q

Mx CAH

A

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

18
Q

Mx precocious puberty

A

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

19
Q

mx of delayed puberty

A

boys:
1 observation
2 3-6 months testosterone

girls:
1 observation
2 3-6 months oestrogen

20
Q

causes of disorders of sexual development

A

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

21
Q

Mx DKA

A

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

22
Q

How do you work out fluid deficit

A

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

23
Q

what are the maintenance fluid requirements in DKA

A

<10kg - 2ml/kg/hr
10-40 - 1ml/kg/hr
40+ - 40ml/hr

lower than usual because of risk of cerebral oedema

24
Q

which fluids should you use in DKA

A

0.9% saline until glucose <14
0.9% saline + 5% glucose when glucose drops below 14
GIVE FLUIDS WITH 40MMOL/L KCL

25
Q

When do you change from IV to SC insulin

A

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

26
Q

monitoring in DKA

A

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)

27
Q

How to manage cerebral oedema in DKA

A

mannitol or hypertonic NaCl

28
Q

How to manage hypokalaemia in DKA

A

<3mmol/L
stop infusion
discuss w/ paediatrc crit care consultant

29
Q

what to discuss with DKA parents

A

factors that led to episode
how to manage intercurrent illness (viral illness)
arrange to see diabetes specialist