1. Correct dehydration over 48 hours (too quickly --> cerebral oedema) 2. Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l. 3. Add potassium to IV fluids and monitor serum potassium closely. 4. Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcutaneous insulin. choice: - “Use 0.9% sodium chloride with 20 mmol potassium chloride in 500 ml (40 mmol per litre) until blood glucose levels are less than 14 mmol/l “ - You would also want to administer IV insulin, but only start this 1-2 hours after administering IV therapy. SC insulin (0.1units/kg/hr)

Paeds endocrine Flashcards by Ailsa Jones

what viruses may trigger T1DM

Coxsackie B virus and enterovirus

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Ideal blood sugar range

4.4 and 6.1 mmol/l

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New diagnosis of T1DM blood tests?

FBC
U&E
Formal laboratory glucose
Blood cultures if ?infection
HbA1c

Thyroid function tests and thyroid peroxidase antibodies (TPO) to test for associated autoimmune thyroid disease

Tissue transglutaminase (anti-TTG) antibodies for associated coeliac disease

Insulin antibodies, anti-GAD antibodies and islet cell antibodies to test for antibodies associated with destruction of the pancreas and the development of type 1 diabetes

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Management hypo in T1diabetes

Rapid acting glucose such as lucozade

+ slower acting carbohydrates such as biscuits or toast to maintain the blood sugar level when the rapid acting glucose is used up

If severe:
IV dextrose and intramuscular glucagon

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Long term complications of hyperglycaemia

macrovascular: CAD, peripheral ischaemia, stroke, HTN
microvascualar: Peripheral neuropathy, Retinopathy, Kidney disease, particularly glomerulosclerosis
infection related : cadidiasis, UTI, pneumonia, skin adn soft tissue infections

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Features DKA

Polyuria
Polydipsia
Dehydration
Nausea and vomiting
Weight loss
Acetone smell to their breath
Altered consciousness
Sepsis (may be underlying trigger)
Potassium imbalance –> arrythmias

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Diagnosing DKA

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)

Ketosis (i.e. blood ketones > 3 mmol/l)

Acidosis (i.e. pH < 7.3)

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DKA management

Correct dehydration over 48 hours (too quickly –> cerebral oedema)
Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l.
Add potassium to IV fluids and monitor serum potassium closely.
Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcutaneous insulin.

choice:
- “Use 0.9% sodium chloride with 20 mmol potassium chloride in 500 ml (40 mmol per litre) until
blood glucose levels are less than 14 mmol/l “
- You would also want to administer IV insulin, but only start this 1-2 hours after administering IV therapy. SC insulin (0.1units/kg/hr)

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Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia and hyperkalaemia

adrenal crisis (addisonian crisis)

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Types of adrenal insufficiency

Primary: autoimmune destruction of adrenal glands –> global depletion in stuff produced by adrenal glands

Secondary: problem with pituitary gland not producing enough ACTH -> reduced stimulation of adrenal gland to produce cortisol

Tertiary: usually caused by long term steroid use (endogenous doesn’t kick in enough)

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Pathophysiology addisons

Autoimmune destruction of adrenal gland –> low cortisol and low aldosterone

High ACTH
Low cortisol
Low aldosterone
High renin

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Pathophysiology secondary adrenal insufficiency

Pituitary gland not producing adequate ACTH –> reduced stimualtion of adrenal glands to produce cortisol –> low cortisol

Low ACTH
Low cortisol
Normal aldosterone
Normal renin

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Investigation addisons? how does it work

Short synacthen test (ACTH stimualtion test)

synthetic ACTH –> stimulate adrenal glands –> if it < doubles then priamry adrenal insufficiency

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features of adrenal insufficiency

Lethargy
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrive

Nausea and vomiting
Poor weight gain or weight loss
Reduced appetite (anorexia)
Abdominal pain
Muscle weakness or cramps
Developmental delay or poor academic performance
Bronze hyperpigmentation to skin in Addison’s caused by high ACTH level

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Investigations adrenal insufficiency

U&Es (hyponatraemia and hyperkalaemia)

blood glucose (hypoglycaemia)

Short synctacten if ?addisons

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Management adrenal insufficiency

Hydrocortisone is a glucocorticoid hormone used to replace cortisol.

Fludrocortisone is a mineralocorticoid hormone used to replace aldosterone if aldosterone is also insufficient.

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Sick day rules adrenal insufficiency

may need to increase steroids (hydrocortisone)

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Management adrenal crisis

Parenteral steroids (i.e. IV hydrocortisone)
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

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puberty stages girls

Boobs
Pubes
Grow
Flow

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puberty stages boys

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Grapes → penis
Drapes
Grow and deepening of voice
Blow

Normal age range for puberty girls and boys

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8 – 14 in girls and 9 – 15 in boys

Define precocious puberty

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‘development of secondary sexual characteristics before 8 years in females and 9 years in males’

thelarche

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the first stage of breast development

adrenarche

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onset of androgen-dependent body changes such as growth of axillary and pubic hair, body odor, and acne

Classifications of precocious puberty

1. Gonadotrophin dependent ('central', 'true') due to premature activation of the hypothalamic-pituitary-gonadal axis FSH & LH raised - CNS tumour - neurofibromatosis type 1 2. Gonadotrophin independent ('pseudo', 'false') due to excess sex hormones FSH & LH low - adrenal tumour/hyperplasia - McCune albright syndrome

pubarche

first pubic hair

What is McCune-Albright syndrome? features?

McCune-Albright syndrome is not inherited, it is due to a random, somatic mutation in the GNAS gene. Features precocious puberty cafe-au-lait spots polyostotic fibrous dysplasia short stature

Causes of delayed puberty?

Hypogonadotrophic - Damage to pituitary/hypothalamus - Growth hormone deficiency - Hypothyroidism - Hyperprolactinaemia - serious chronic conditions - excessive exercise - Kallman syndrome Hypogonadism - Previous damage to the gonads - Congenital absence of the testes or ovaries - Kleinfelter’s Syndrome (XXY) - Turner’s Syndrome (XO)

What is kallman syndrome

Kallman syndrome is a inherited genetic condition causing hypogonadotrophic hypogonadism, resulting in failure to start puberty. It is associated with a reduced or absent sense of smell (anosmia)

threshold for initiating investigations for delayed puberty

No evidence of pubertal changes in a girl aged 13 or a boy aged 14 or girl 15 with secondary but no period

Presentation growth hormone deficiency

Neonates: Micropenis Hypoglycaemia Severe jaundice Older children Poor growth, usually stopping or severely slowing from age 2-3 Short stature Slow development of movement and strength Delayed puberty

pharmacological name growth hormone

somatropin

What is the growth hormone stimualtion test

Measuring effect of medications that normally stimulate the release of growth hormone. Examples of these medications include glucagon, insulin, arginine and clonidine. Growth hormone levels are monitored regularly for 2-4 hours after administering the medication to assess the hormonal response. In growth hormone deficiency there will be a poor response to stimulation.

Presentation congenital hypothyroid

tested for on blood spot Prolonged neonatal jaundice Poor feeding Constipation Increased sleeping Reduced activity Slow growth and development

Types of diabetes insipidus and pathophysiology

Cranial Nephrogenic

Water deprivation test

1. avoid fluid for 8 hours 2. measure urine osmolarity 3. give synthetic ADH 4. 8 hours later measure osmolarity again after dep after ADH Cranial low high Nephrogenic low low Priamry high high

Management cranial DI

desmopressin

Management nephrogenic DI

thiazides, low salt/protein diet

Invetsigation DI

water deprivation test

Bicarbonate level in DKA?

low as ketones are using it up

Fluid specifics DKA

IV fluids (0.9% NaCl 10ml/kg) + SC insulin (0.1units/kg/hr)

creatinine level DKA

mildly raised as dehydrated

How is fluid resus different if shocked or not shocked?

If shocked: do NOT subtract bolus from rest If not shocked: subtract bolus later

DKA severity

pH < 7.1 severe DKA (10% dehydration) pH <7.2 moderate DKA (5% dehydration) pH<7.3 mild DKA not dehydrated

normal range bicarbonate

22-29 mEq/L

normal blood pH

7.35 to 7.45, with the average at 7.40

What to do if you suspect T1 diabetes but not DKA

suspect if random blood glucose > 11 mmol refer for immediate same day assessment

Management cerebral oedema DKA

* Hypertonic saline (2.7% or 3% saline. 2.5-5ml/kg over 10-15min) or * Mannitol (20% 0.5-1g/kg over 10-15min)

what is conns syndrome?

hyperaldosteronism (high aldosterone) either due to primary or secondary

Paeds endocrine Flashcards

(49 cards)