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Toni's Paeds > Endo > Flashcards

Endo Flashcards

1
Q

What chance does an identical twin of a diabetic have of developing the disease?

A

30-40%

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2
Q

What is the risk of developing T1DM in the general population?

A

1/400

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3
Q

What is the risk of developing T1DM if your mother has it?

A

1/40-80

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4
Q

What is th risk of developing T1DM if your father has it?

A

1/20-40

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5
Q

What might trigger development of T1DM?

A

enteroviral infections

cows milk protein

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6
Q

What causes T1DM

A

AI process
-> pancreatic beta cell destruction
insulin deficiency

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7
Q

What are markers of bet cell destruction?

A

islet cell antibodies

glutamic acid decarboxylase antibodies

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8
Q

When are the two age peaks and two seasonal peaks in T1DM presentation?

A

preschool
teenager
spring
autumn

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9
Q

What is the classical paediatric presentation of T1DM

A

polydipsia
polyuria
weight loss
nocturnal enuresis

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10
Q

What are rarer presenting features of T1DM in paeds?

A

skin sepsis

candida infection

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11
Q

Symptoms and Signs of DKA

A 
abdo pain
vomiting
dehydration (can -> shock)
hyperventilation
drowsiness (can -> coma)
sell of ketones on breath
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12
Q

How to confirm diagnosis of T1DM

A

random blood glucose >11.1
fasting blood glucose >7
glycosuria
ketonuria

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13
Q

When might you suspect T2DM in a child?

A

fhx T2DM
severely obese
acanthosis nigricans
PCOS phenotype

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14
Q

What does diabetes education involve?

A 
Pathophysiology of T1DM
Insulin injection: sites + technique
Diet advice: carb counting
Adjusting for exercise
Sick-day rules
Blood glucose + ketones monitoring
Recognising and treating hypos
Psych impact
Sources of support
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15
Q

Who comprise the diabetes MDT?

A 
Paeds consultant
Paeds diabetic specialist nurse
Paeds dietician
Clinical osychologist
Social worker
Support groups
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16
Q

Rapid-acting human insulin analgues

A

insulin lispro: Humalog
insulin glulisine: Apidra
insulin aspart: Novo Rapid

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17
Q

Long-acting human insulin analogues

A

insulin detemir: Levemir

glargine: :antus

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18
Q

Short-acting soluble human regulator insulin

A 
Actrapid
Humulin 5
30-60 min onset of action 
8 hr duration
given 15-30 min prior to meals
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19
Q

intermediate-acting insulin

A

Insulatard
Humulin I
1-2 hr onset
peak action 4-12 hrs

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20
Q

insulin injection sites

A 
sub cutaneous:
upper arm
buttocks
abdomen
ant + lat thigh
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21
Q

What insulin regimens are there?

A

basal-bolus regimen

continuous pump insulin

22
Q

what are the factors which affect insulin dosage?

A 
age
weight
diet
blood glucose
exercise
infection/illness
hormones e.g. puberty
23
Q

What is HbA1c?

A

glycosylated haemoglobin
indicates control over 6-12 wks
check 3x yearly

24
Q

What are the symptoms of hypoglycaemia?

A

Asymptomatic
Jittery, convulsions, hypotonia, apnoea
Blood glucose

25
Q

What are the causes of congenital hypothyroidism?

A

maldescent of the thyroid/athyrosis
dyshormonogenesis
iodine deficiency
TSH deficiency

26
Q

What is maldescent / athyosis?

A

commonest cause of sporadic congenital hypothyroidism
failure of thyroid to migrate from base of tongue to subpharyngeal position
partial/complete failure of thyroid development

27
Q

What is dyshormogenesis?

A

inborn error of thyroid hormone synthesis

more likely with consanguinous parents

28
Q

What is iodine deficiency congenital hypothyroidism?

A

commonest cause worldwide

prevented by iodination of salt in the diet

29
Q

What is TSH deficiency congenital hypothyroidism?

A

rare

30
Q

What are the clinical features of congenital hypothyroidism?

A

failure to thrive, feeding issues, prolonged jaundice, constipation, pale mottled dry skin, large tongue, hoarse cry, coarse facies, goitre, umbilical hernia, delayed development

31
Q

What are the clinical features of acquired hypothyroidism?

A

female>male, short stature, cold intolerance, dry skin, bradycardia, goitre, slow relaxing reflexes, contipation, delayed puberty, slipped upper femoral epiphysis, learning difficulties
Usually AI: Hashimoto’s
Autoantibodies to thyroid peroxidase found

32
Q

What is juvenile hypothyroidism?

A

due to AI thyroiditis
incr risk in Downs or Turners
incr risk of other AI diseases
goitre often present

33
Q

What is hyperthyroidism

A

oft due to Graves AI thyroiditis
secondary to thyroid stimulating immunoglobulins
teenage girls
1st line: carbimazole

34
Q

What is the treatment for hyperthyroidism?

A

Carbimazole

+ beta blockers for symptomatic relief

35
Q

Side effects of steroids

A 
Htn
Glucose intolerance - hyperglycaemia
Weight gain: tray all obesity, intra scapular fat pad
Short stature
Osteoporosis
Striae, thin skin + incr bruising
Prox myopathy
Incr susceptibility to infection
Adrenal suppression
Cataracts
36
Q

Precocious puberty

A

Onset of puberty: girls boys, 80-90% idiopathic, other = intracranial pathology
False= inappropriate sequence = gonadotrophin independent, extracranial: CAH, Cushing’s, malignancy,
McCuneAlbright: + cafe au lait spots + fibrous dysplasia

37
Q

Treating an addisonian crisis

A

Hydrocortisone

IV dextrose

38
Q

McCune Albright syndrome

A

Sporadic genetic condition
Precocious puberty: primary ovarian cysts secreting oestradiol
Cafe au last spots
Polyostotic fibrous dysplasia: normal bone replaced by cystic bone

39
Q

Delayed puberty

A 
Absence of pubertal development
Girls 13 yrs
Boys 14 yrs
Or failure of progression over 2 yrs
1st line investigation: gonadotrophins
40
Q

Measures to take when changing insulin regime

A

Adjust only one dose at a time
Increase or decrease dose by 10%
Allow a few days to assess outcome
Check blood sugar more regularly

41
Q

Growth hormone deficiency

A

Drop in growth velocity
Assoc with neonatal hypoglycaemia, jaundice, doll-like face
Acquired causes: head injury, irradiation + tumours
Congenital: inherited, idiopathic, assoc with midline defects e.g. cleft palate
Treatment: GH supplementation

42
Q

Causes of delayed puberty

A 
Low gonadotrophins:
Constitutional delay, chronic illness(CF, asthma, crohns, anorexia), disorders of the hypothalamic-pituitary axis, intracranial lesions. 
Raised gonadotrophins + defective gonads
Turners, Klinefelter's
Chemo/radiotherapy
Torsion
43
Q

Causes of cranial diabetes insipidus

A

Head injury
Surgery
Sarcoidosis
DIDMOAD: diabetes insipidus, diabetes mellitus, optic atrophy, deafness

44
Q

Causes of nephrogenic diabetes insipidus

A

Metabolic abnormalities: hypokalaemia, hypercalcaemia
Drugs: lithium, demeclocycline
Genetic defects
Heavy metal poisoning

45
Q

Which infants are at greater risk of hypoglycaemia?

A

Babies

46
Q

What are the risks of untreated hypoglycaemia?

A

Permanent neurological disability

Management: feed or IV glucose if not possible

47
Q

What is Cushing’s syndrome?

A

Clinical features due to adrenal steroid excess
Most commonly caused by iatrogenic steroids
Moon-like facies, plethora, acne
Interscapular fat pad, truncal obesity, growth arrest
Easy bruising, htn, hypogonadism, cataracts, glucose intolerance
Raised 24 hr free urinary cortisol
Or dexamethasone suppression test

48
Q

What is Cushing’s disease?

A

Excess corticosteroid secretion secondary to a pituitary tumour
May present with features of Cushing’s syndrome

49
Q

What is Addison’s disease?

A

Primary AI mediated adrenocortical failure:
Decr glucocorticoids= hypoglycaemia, weight loss
Decr mineralocorticoids= hypotension, hyperK, hypoNa
Decr adrenal androgens= decr body hair + libido
ACTH excess= incr pigmentation

50
Q

How is Addison’s disease diagnosed?

A

Short synthACTHen test: no rise in cortisol
Management: replace glucocorticoids + mineralocorticoids
With hydrocortisone + fludrocortisone

Toni's Paeds (16 decks)

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