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Finals Systems > Paeds endocrine > Flashcards

Paeds endocrine Flashcards

1
Q

what viruses may trigger T1DM

A

Coxsackie B virus and enterovirus

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2
Q

Ideal blood sugar range

A

4.4 and 6.1 mmol/l

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3
Q

New diagnosis of T1DM blood tests?

A

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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4
Q

Management hypo in T1diabetes

A
  1. 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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5
Q

Long term complications of hyperglycaemia

A
  1. macrovascular: CAD, peripheral ischaemia, stroke, HTN
  2. microvascualar: Peripheral neuropathy, Retinopathy, Kidney disease, particularly glomerulosclerosis
  3. infection related : cadidiasis, UTI, pneumonia, skin adn soft tissue infections
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6
Q

Features DKA

A

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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7
Q

Diagnosing DKA

A

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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8
Q

DKA management

A
  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)

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9
Q

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia and hyperkalaemia

A

adrenal crisis (addisonian crisis)

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10
Q

Types of adrenal insufficiency

A

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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11
Q

Pathophysiology addisons

A

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

High ACTH
Low cortisol
Low aldosterone
High renin

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12
Q

Pathophysiology secondary adrenal insufficiency

A

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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13
Q

Investigation addisons? how does it work

A

Short synacthen test (ACTH stimualtion test)

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

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14
Q

features of adrenal insufficiency

A

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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15
Q

Investigations adrenal insufficiency

A

U&Es (hyponatraemia and hyperkalaemia)

blood glucose (hypoglycaemia)

Short synctacten if ?addisons

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16
Q

Management adrenal insufficiency

A

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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17
Q

Sick day rules adrenal insufficiency

A

may need to increase steroids (hydrocortisone)

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18
Q

Management adrenal crisis

A

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

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19
Q

puberty stages girls

A

Boobs
Pubes
Grow
Flow

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20
Q

puberty stages boys

A

Grapes → penis
Drapes
Grow and deepening of voice
Blow

21
Q

Normal age range for puberty girls and boys

A

8 – 14 in girls and 9 – 15 in boys

22
Q

Define precocious puberty

A

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

23
Q

thelarche

A

the first stage of breast development

24
Q

adrenarche

A

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

25
Q

Classifications of precocious puberty

A
  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
26
Q

pubarche

A

first pubic hair

27
Q

What is McCune-Albright syndrome? features?

A

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

28
Q

Causes of delayed puberty?

A

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)

29
Q

What is kallman syndrome

A

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)

30
Q

threshold for initiating investigations for delayed puberty

A

No evidence of pubertal changes in a girl aged 13 or a boy aged 14

or girl 15 with secondary but no period

31
Q

Presentation growth hormone deficiency

A

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

32
Q

pharmacological name growth hormone

A

somatropin

33
Q

What is the growth hormone stimualtion test

A

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.

34
Q

Presentation congenital hypothyroid

A

tested for on blood spot

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

35
Q

Types of diabetes insipidus and pathophysiology

A

Cranial

Nephrogenic

36
Q

Water deprivation test

A
  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
37
Q

Management cranial DI

A

desmopressin

38
Q

Management nephrogenic DI

A

thiazides, low salt/protein diet

39
Q

Invetsigation DI

A

water deprivation test

40
Q

Bicarbonate level in DKA?

A

low as ketones are using it up

41
Q

Fluid specifics DKA

A

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

42
Q

creatinine level DKA

A

mildly raised as dehydrated

43
Q

How is fluid resus different if shocked or not shocked?

A

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

44
Q

DKA severity

A

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

45
Q

normal range bicarbonate

A

22-29 mEq/L

46
Q

normal blood pH

A

7.35 to 7.45, with the average at 7.40

47
Q

What to do if you suspect T1 diabetes but not DKA

A

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

48
Q

Management cerebral oedema DKA

A
  • Hypertonic saline (2.7% or 3% saline. 2.5-5ml/kg over 10-15min)

or

  • Mannitol (20% 0.5-1g/kg over 10-15min)
49
Q

what is conns syndrome?

A

hyperaldosteronism (high aldosterone)

either due to primary or secondary

Finals Systems (27 decks)

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