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Peadiatrics > Endocrine And Metabolic Disordersm > Flashcards

Endocrine And Metabolic Disordersm Flashcards

1
Q

What causes type 1 diabetes

A

Deficient insulin due to T-cell mediated autoimmune destruction of B-cells in pancreatic islets of langerhans

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2
Q

How much destruction of B cells for T1DM to become clinically significant ?

A

90%

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3
Q

What happens when blood glucose levels exceed renal threshold?

A

Osmotic diuresis - increased urination due to increased substances that can’t be reabsorbed eg. Glucose

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4
Q

What are the 3 key clinical features of T1DM ?

A

Polyuria
Polydipsia
Weight loss

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5
Q

Diagnosis of type 1 DM

A

Symptomatic child with random blood glucose >11mmol/L (+/-glycosuria/ketouria)

If doubt - glucose tolerance test -> fasting glucose >7mmol/L

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6
Q

4 parts of management for type 1 diabetes

A

Insulin replacement
Diet and exercise
Monitoring
Education & psychological support

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7
Q

Why do you need less insulin initially after diagnosis of T1DM ? What is the average requirement

A

Honeymoon period while remaining Bcells are destroyed

0.5-1 unit/Kg/day

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8
Q

Eg of insulin regimes

A

Twice daily
Basal bolus
Continuous pump infusion

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9
Q

How does a twice daily regime work with insulin

A

Total daily dose split 1:2 between short acting and Medium acting insulin.
2/3 in breakfast injection
1/3 in evening injection

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10
Q

What happens in a basal bolus injection

A

Multiple daily injections of short acting insulin and once daily long acting (glargine / detemir) to provide a background

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11
Q

What is continuous pump infusion insulin

A

Subcutaneous insulin infusion SII

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12
Q

Where is insulin injected and why

A

*Subcutaneously into upper arms, outer thighs or abdomen

Sites should be related to decreased risk of lypohypertrophy & atrophy *

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13
Q

What foods should be eaten in diabetes ? What pattern of eating ? When should food intake increase and why?

A

High fibre, complex carbohydrates as these give sustained release of glucose (avoid refined carbs eg. Sweets)
3 even main meals with snacks
After exercise to avoid hypoglycaemia

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14
Q

When should blood glucose be tested ? What is the aim level?

A

Morning and evening and before meals

4-6mmol/L

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15
Q

What other than blood glucose should be monitored? What level do you want it at

A

HBA1C

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16
Q

What are two risks with adolescents who have diabetes ?

A

Increase demand in monitoring

Risk of non compliance

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17
Q

What needs to be taught to diabetics ? Eg of voluntary group to support ?

A

Injection of insulin - technique and sites, monitoring

Diabetes UK

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18
Q

Clinical features of DKA (9 things)

A

Vomiting, dehydration, abdo pain, hyperventilation due to acidosis, kussmaul breathing, drowsiness, acetone smell on breath, coma, hypovolaemic shock

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19
Q

What investigations should be done in DKA ? What results ?

A

Blood glucose - >11mmol
U&E, creatinine - dehydration
ABG - metabolic acidosis (ph

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20
Q

What are the ECG changes in hypokalaemia

A

t wave inverted / flattened

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21
Q

Management of severe DKA

A

*Fluid - 10mls/kg normal saline, then replace
Insulin - 0.05-0.1 units /kg/ hour
Potassium - initiate as soon as urine passed *
Reestablish oral fluids, SC insulin & diet
Identify and treat underlying cause (eg. Infection, steroids, puberty)

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22
Q

Why is HCO3 not indicated to treat acidosis

A

Self corrects with insulin and fluid

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23
Q

What 3 things can kill a child in DKA

A

Cerebral oedema
Hypokalaemia
Aspiration pneumonia

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24
Q

When do you get symptoms with hypoglycaemia ? What are the symptoms? How do you treat ?

A

seizures / coma)

Sugary drink, glucose tablet or buccal gel

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25
Q

What are the clinical features of congential hypothyroidism

A 
Prolonged neonatal jaundice
Feeding problems
Constipation
Large fontanelle, tongue, goitre 
Hypotonia
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26
Q

What are the 3 causes of congenital hypothyroidism

A

Athyrosis / maldescent (?sublingal)
Dyshormogenesis - error of TH synthesis
Maternal iodine deficiency

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27
Q

Where are rates of dyshormogenesis present ? What’s usually on baby?

A

Consanguineous pedigree

Goitre

28
Q

Diagnosis and treatment of hypothyroidism

A

Increased TSH

Thyroxine

29
Q

When can hyperthyroidism be congential? What’s common cause in childhood? Who gets the most?

A

Mother with graves

Graves - teenage girls most common

30
Q

Diagnosis of hyperthyroidism

A

Increased t3/ t4
Decreased TSH
Antimicrosomal antibodies

31
Q

Treatment of hyperthyroidism ? If there is a relapse ?

A

Carbimazole is 1st line (+B-blockers for symtomatic relief)

Sub total thyroidectomy or radioiodine can be used if relapse after treatment

32
Q

When should you check for hyperthyroidism

A

Deteriorating school performance

Delayed / accelerated puberty

33
Q

3 causes of adrenocortical insufficiency

A

Congenital adrenal hyperplasia
1^ adrenal cortical insufficiency - addisons
2^ adrenal cortical insufficiency - cushings (pit adenoma) / syndrome (usually iatrogenic)

34
Q

Genetics of congential adrenal hyperplasia? What is it?

A

90% clauses by deficient 21-hydroxylase, autosomal recessive
Group of disorders chased by defect in production of cortisol from cholesterol

35
Q

What causes features of CAH ? What are they? Why?

A

Androgen excess
Female virilization
Salt crises due to mineral corticoid deficiency (decreased circulating volume, electrolyte imbalance, shock)
cortisol deficiency (hypoglycaemia, hypotension, shock)

36
Q

Diagnosis of CAH

A

Elevated serum 17a-hydroxyprogesterone

37
Q

How do you manage a salt losing crisis of CAH

A

Volume replacement with normal saline and systemic steroids

38
Q

Long term management of CAH

A

Cortisol replacement with hydrocortisone

Mineral corticoid replacement with fludrocortisone if there is salt wasting

39
Q

What causes addisons ?

A

autoimmune disease, haemorrhage & infarction, TB

40
Q

What is addisons caused by haemorrhage and infarction called

A

Waterhouse-friderichsen syndrome

41
Q

Features of addisons

A

Postural hypotension and increased pigmentation

42
Q

What is intercurrent illness ? What can happen with addisons ?

A

Illness while you have another illness

Adrenal crisis -> vomiting, dehydration, shock

43
Q

What is Cushing’s syndrome? Causes?

A

Glucocorticoid excess
Primary - adrenal tumours
Secondary - ACTH secretion from pituitary adenoma / ectopic source
Iatrogenic - long term glucocorticoid use (eg. Nephrotic syndrome)

44
Q

Features of cushings

A

Short stature , truncal deformity (buffalo hump), rounded moon face, hypertension, signs of virilization

45
Q

2 parts of diagnosis for cushings

A

Elevated serum cortisol with normal diurnal rhythm (high midnight levels*)
dexamethasone suppression test

46
Q

What’s it for? And What happens in a dexamethasone suppression test ?

A

Determine cushings disease vs syndrome

Disease - bilateral adrenal hyperplasia due to pituitary increased ACTH - SUPPRESSED

syndrome - eg. Tumour of adrenal/iatrogenic - NOT SUPPRESSED

47
Q

Is deficiency or excess more common in ant pituitary? Wh of causes?

A

Deficiency
Cranial defects - eg. Agenesis of corpus callosum
Tumours - eg. Cranialpharyngioma
Idiopathic hormone abnormalities

48
Q

What is a craniopharyngioma

A

Brain tumour from pituitary embryonic tissue

49
Q

Features of hypopituitarism

A

Growth retardation common

Adrenal, thyroid, gonadal dysfunction

50
Q

2 disorders due to posterior pituitary

A

Diabetes insipidus

Syndrome of inappropriate secretion of ADH

51
Q

What causes central diabetes insipidus

A

ADH deficiency

Can occur in isolation / with anterior pituitary deficiency (eg tumours, infection, trauma)

52
Q

How does diabetes insipidus present ? What are the DDs?

A

Polydipsia , Polyuria

Hypercalcaemia, CKD, type 1 diabetes, psychogenic water drinking

53
Q

Diagnosis of SIADH

A

hypo osmolality with hyponatraemia
Normal renal, thyroid and adrenal function
Normal or increased volume status (HTN)
Elevated urine sodium osmolality

54
Q

What causes symptoms in SIADH ? What are they?

A

Water intoxication

Seizures, behavioural changes, vomiting

55
Q

What causes SIADH ? Why?

A

Common stress response

CNS disease - meningitis, tumours, trauma
Lung disease - pneumonia

56
Q

What causes phenylketonuria ?

A

Autosomal recessive

defective phenylalanine hydroxylase

57
Q

What does phenylalanine hydroxylase usually do? What happens when it’s defective and this doesn’t happen?

A

Converts phenylalanine to tyrosine.

Phenylalanine builds up and by-products (eg. Phenylacetic acid) build up and are excreted in the urine -> “PKU”

58
Q

Features of phenylketonuria ? Neuro, growth, hypopigmentation

A

Neuro - Moderate / severe mental retardation, hypertonia, tremors, behavioural disorders

Growth - slowed

Hypopigmentation - fair skinned, light haired

59
Q

Why do you get hypopigmentation in phemylketouria

A

Tyrosine is required to form melanin

60
Q

Treatment of phenyketouria

A

Decreased Phenylalanine in diet until at least 6 years

61
Q

What are the features of glalactosaemia ? When should it be tested for? How is the diagnosis made ?

A

Neonatal liver dysfunction, coagulopathy & cataracts
Severe neonatal jaundice

Reducing substances found in urine

62
Q

What happens in glycogen storage diseases ? Features?

A

Abnormal accumulation of glycogen in tissues

Growth failure, hypoglycaemia, hepatomegally

63
Q

What is mucopolysaccharidoses (MPS) ?

A

Progressive multiply stem disorders that can affect CNS, heart, eyes, and skeleton

64
Q

What are the features of MPS

A

Developmental delay in first year

Coarse faces - normal at birth but develop in most cases

65
Q

Treatment of MPS

A

Bone marrow transplant

66
Q

What are coarse faces seen in? What are features?

A

Inborn errors of metabolism ( MPS, phenylketonuria)

Large head, prominent veins, flat nose, big lips

Peadiatrics (14 decks)

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