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Paediatrics > Growth/endocrine/metabolic/nutrition > Flashcards

Growth/endocrine/metabolic/nutrition Flashcards

1
Q

What could secondary nocturnal enuresis be caused by?

A

Young children may present this way at first presentation of IDDM

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2
Q

What two other chronic conditions is type I DM associated with?

A

coeliac’s and hypothyroidism

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3
Q

Recommend an insulin regimen for a young child

A

Twice daily - mixture of short and long-acting (30:70 respectively) - 2/3 before breakfast, 1/3 before dinner

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4
Q

What are the symptoms of DKA?

A 
Polyuria
Vomiting
Abdominal Pain
Tachypnoea
Drowsiness, confusion, coma
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5
Q

What long-term complications should you warn about when diagnosing IDDM?

A

Retinopathy
Nephropathy
Heart disease
Neuropathy

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6
Q

In a symptomatic individual what levels of blood glucose would be diagnostic of DM?

A

Fasting >7mmol/L

Random > 11.1 mmol/L

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7
Q

What pH level indicates severe DKA? How does this affect the management?

A

pH <7.1
It affects the presumed fluid deficit the patient has - in severe it is 10% of the patients bodyweight (in moderate/pH<7.3 it is 5% of the patients bodyweight)

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8
Q

What fluid bolus should be given to a patient in DKA and shock? When should insulin be given?

A

10ml/kg of 0.9%NaCl
Thereafter any fluids should contain KCl as insulin will drive the potassium into the cells

Insulin should be given 1-2 hours post-fluids (0.05-0.1 U/kg/hr)

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9
Q

What should a parent do in the event of hypoglycaemia?

A

If conscious give carb containing snack or dextrose tablet
If unable to eat/drink - rub buccal glucose gel
If unconscious give IM glucagon

Get medical help ASAP

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10
Q

When should a child be hospitalised for FTT?

A

Severe (fall of 3 centiles)
<6mo old
Requiring active refeeding
Serious underlying condition that requires investigation

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11
Q

What investigations should be done in a child presenting with FTT?

A 
Bloods - FBC and ferratin (anaemia from coeliac's)
TFTs - hyperthyroidism
CRP, ESR - IBD
Sweat test - CF
MSU - IDDM
Skeletal survey - dwarfism, abuse
DNA PCR if suspect genetic condition
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12
Q

If a young child is found to be >98th centile in weight what is he classed as?

A

obese

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13
Q

Why is sleep important in managing obesity?

A

Sleep deprivation –> low leptin and high ghrelin –> low fullness/high hunger
Sleep apnoeas - ask about snoring and lethargy/tiredness during day

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14
Q

How might hypothyroidism present in a baby?

A 
poor feeding and FTT
Prolonge jaundice
Constipation
pale, cold, mottled baby
Large tongue
Coarse facies
Umbilical hernia
Goitre (rare)
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15
Q

What is the most common aetiology of congenital hypothyroidism?

A

Maldescent of the thyroid - stays just below the tongue

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16
Q

When is a diagnosis of congenital hypothyroidism (cretinism) normally made?

A

Guthrie/heelprick test

Start thyroxine replacement ASAP

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17
Q

What investigations should be done when a child presents with short stature?

A

Monitor growth - growth chart
Measure parents height and discern mid-height (mean of both parents height +/- 7 (+ for boys, - for girls)
Imaging - x-ray of wrist to see development of carpal bones
Bloods to investigate pathological cause - e.g. CRP/ESR for IBD

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18
Q

What are the two types of phenylketonuria?

A

Inborn error of of phenylalanine hydroxylase (good prognosis)
Inborn error of biopterin metabolism (worse prognosis)

Results in accumulation of phenylalanine in the tissues

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19
Q

Management of phenylketonuria?

A

lifelong diet low in phenylalanine (found in protein containing foods - beef, pork, poultry, eggs, cheese etc.)

Regular monitoring of phenylalanine levels - important in pregnant women as high phenylalanine levels are very detrimental to foetus

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20
Q

What is congenital adrenal hyperplasia?

A

Autosomal recessive disorder - 21-hydroxylase deficiency - converts precursors of cortisol and aldosgterone –> high levels of ACTH –> high levels of testosterone

80% = salt losers - vomiting, weight loss, floppiness (adrenal crisis) - hyponatraemic, hypoglycemic, hyperkalaemia

Presents as ambiguous genetalia

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21
Q

Normal puberty?

A 
Male = 10-14
Female = 8.5-12
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22
Q

What condition would be most likely to delay puberty in a female?

A

Turners - 45,X

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23
Q

How would you treat delayed puberty in a male?

A

Oxandolone in a younger patient

Testosterone if older patients

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24
Q

Describe a typical childhood absence seizure case

A

age 3-12yrs
Absence seizure lasting 5-20 seconds - can be precipitated by hyperventilation and has associated automatisms e.g. lip smacking or eye-lid flickering

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25
Q

Management of childhood absence seizures?

A

95% remission in adolescence
Can give sodium valproate
Avoid carbamazepine - exacerbates seizures

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26
Q

Describe a typical juvenile myoclonic epilepsy case

A

Teenage girl - exacerbated by lack of sleep, alcohol and flashing lights
Random myoclonic jerks of the upper limb, usually in the morning
Generalised tonic-clonic +/- absence seizures

Drug of choice = sodium valproate

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27
Q

Describe a case of benign Rolandic epilepsy

A

9 year old (onset 3-12 years)
Nocturnal, benign seizures - paraesthesia of face unilateral side and facial motor seizure of ipsilateral side
No LOC but unable to speak (aphasia), often with salivation
Drugs usually not needed

28
Q

What is an infantile spasm?

A

Onset usually 4-6 months
Violent flexor spasm (trunk and head - 2 secs) followed by arm extension (20-30secs)
EEG shows hyperarrythmia with high voltage and slow wave
Management - Vigabatrin and corticosteroids

29
Q

What is Lennox-Gastaut Syndrome?

A

Triad of:
Infantile spasm
Motor regression
Characteristic EEG - asynchronous spikes on chaotic background

Leads to developmental delay and persistent seizures

5%mortality
Management = Vigabatrin + steroids + ACTH

30
Q

General treatment principles of childhood epilepsy?

A

Tonic-clonic and partials:
First line: sodium valproate +/- carbamazepine
Second line: Lamotrigine

Ketogenic diet may help children with difficult seizures

Withdrawal: done slowly after >2 years without seizures

31
Q

What are breath holding attacks?

A

In toddlers - upset child –> holds breath –> turns blue +/- LOC –> rapid recovery

No drugs required, avoid confrontation

32
Q

What are reflexic anoxic seizures?

A

Brief episodes of asytole triggered by pain, fear and anxiety
–> pale, limp and LOC –> tonic-clonic phase
Episodes last 30-60 secs, child will feel tired afterwards

Most commonly between 6mo-2yrs

33
Q

What type of migraine do children normally get?

A

Migraine without aura - pulsatile headache in the termporal/frontal region (usually bilateral) which is often accompanied by N+V+abdo pain and/or photo/phonophobia

Relieved by rest

34
Q

What common drug is contraindicated when a patient suffers from migraine with aura?

A

OCP

35
Q

How can an aura present?

A

Visual disturbance:
Positive phenomena - zig-zags
Negative phenomena - lose part of vision

Auditory disturbance
Awareness headache is imminent (<1hr)

36
Q

Management of migraines?

A

Lifestyle - avoid triggers and promote healthy lifestyle (e.g. adequate sleep)

Analgesia - paracetamol –> codeine
+/- antiemetic e.g. metaclopramide, prochlorperazine
Seratonin (5HT) antagonist e.g. Sumatriptan (intranasal for >12 yrs

Prophylaxis - B-blockers - proanolol

37
Q

Where does the problem lie in communicating hydrocephalus?

A

The arachnoid villi - failure to reabsorb CSF

Caused by SAH or meningitis

38
Q

What are the causes of non-communicating hydrocephalus?

A

Congenital:
Chiari malformation - brain/cerebellum extend into foramen magnum
Dandy-walker malformation - blocked 4th ventricle outflow
Aqueduct stenosis

Posterior fossa neoplasms
Vascular malformation
Intraventricular haemorrhage (preterm)

39
Q

Signs of hydrocephalus?

A

Enlarged head circumferecne with frontal bossing, distention of scalp veins +/- ‘setting sun’ eyes

Separation of skull sutures with bulging fontanelle
Hyperreflexia
Spasticity

40
Q

management of hydrocephalus?

A

Address the cause

Ventriculoperitoneal shunt allows drainage of excess fluid
NB. infection risk, can get blocked, low pressure headaches (mostly prevented by valve)

41
Q

How does a SAH present? what is the management?

A

Acute onset of headache, neck stiffness +/- fever
May develop –> seizure and coma

Signs = retinal haemorrhage
CT - blood in CSF, avoid doing a LP

Management - surgery or interventional radiology

42
Q

How does a extradural haemorrhage present? what is the management?

A

Cause = trauma - associated with skull fracture and bleed from middle meningeal artery

Reduced conscious level +/- seizures (may be preceded by period of lucidity)
Infants may present with anaemia and shock
There may be focal neurological signs = dilated ipsilateral pupil, contralateral limb paresis

management = Correct hypovolemia, surgery referral

43
Q

What is a classic cause of subdural haematoma?

A

Non-accidental injury i.e. shaking or direct trauma

Look for retinal haemorrhage

44
Q

How does a subdural haemorrhage present? what is the management?

A

Increasing headache and confusion
Retinal haemorrhage

management: CT head
Craniotomy and evacuation

45
Q

What is Duchenne’s Muscular Dystrophy?

A

X-linked recessive disorder (1 in 4000 males) characterised by progressive and eventually lethal muscle dysfunction (prognosis = late 20’s)

Deletion of X chromosome = no dystrophin –> progressive muscular wasting

Sub-type = Becker muscular dystrophy - some dystrophin produced so better prognosis (death at 40)

46
Q

Symptoms of Duchenne’s?

A

Clumsy weak child with a waddling gait (+/- language delay)
Slow running, difficulty with stairs
Eventually –> respiratory failure and cardiomyopathy

47
Q

Signs of Duchenne’s?

A

Gower’s sign = stands up with arms on legs (NB. normal in children <3 yrs)
Joint contractures and scoliosis
pseudo hypertrophy of calves - fat takes place of muscle

48
Q

Investigations into Duchenne’s?

A

Bloods - CPK very high (creatinine phosphokinase)
DNA assays
Muscle biopsy

49
Q

Aetiology of neural tube defects?

A

Failure of neural tube closure in first 28 days after conception
Incidence greatly reduced in last 30-40 years because of improved nutrition an folic acid supplementation

50
Q

Presentation of spina bifida occulta?

A

Failure of the vertebral arch to close but spinal cord remains in torso
Presents with overlying skin lesion with tuft of hair
Bowel/bladder function may be affected - normally incidental finding
No management usually required - unless tethering of spinal cord

51
Q

Presentation of meningocele?

A

Protrusion of meninges outside of body with overlying skin - swelling on back

Management = surgical repair

52
Q

Presentation of myelomeningocoele?

A

Failure of vertebral arch, spinal cord and meninges to close
Protrusion of exposed spinal cord +/- imperforate anus

Associated with:
leg imbalance
Sensory loss
Bladder/bowel denervation
Scoliosis
53
Q

Presentation of anencephaly?

A

Incomplete closure of neural plate ~21 days –> incomplete skull/brain development
Exposed brain tissue at birth
Babies die within first week

54
Q

Presentation of encephalocoele?

A

Incomplete closure of neural plate ~25 days –> failure of posterior skull to close –> herniation of brain tissue into sac
Skin covered sac on back of neck - requires surgical correction
Complication = poor neurological development

55
Q

What is plagiocephaly and what is it caused by?

A

Flat head syndrome

Cause: Excessive lying down supine - higher prevalence amongst ‘floppy babies’

56
Q

management of plagiocephaly?

A

cranial remoulding head bands

Will improve as baby becoems more mobile

57
Q

Causes of malnutrition?

A

Inadequate intake
Inadequate retention - vomiting, eating disorder
Malabsorption - IBD, coeliac
Increased requirement - chronic illness

58
Q

Assessment of nutrition?

A

Diet diary
Antropometry - height, weight, upper arm circumference, triceps skin fold thickness
Bloods - albumin, vitamins/minerals (e.g. Fe), immunodeficiency (reduced WCC)

Bloods - glucose, U+E’s, LFTs

59
Q

What are wasted and stunted growth patterns?

A

Wasted = 70% weight/age, 70% weight/height

Stunted 70% weight/age, 85% height/age

60
Q

Presentations of malnutrition?

A

Marasmus - wasted/wisened appearance, apathetic

kwashiokor - oedema, sparse and depigmentated hair, angular stomatitis, diarrhoea, distended abdomen, hepatomegaly

61
Q

management of malnutrition?

A

Correct hypoglycemia, dehydration and hypothermia
Correct electrolytes
Correct mineral/vitamin deficiency
Parenteral feeds - NG tube (beware of re-feeding syndrome)

62
Q

What is rickets caused by?

A

Vit D deficiency –> increased bone resorption

inadequate dietary intake (breast fed exclusively for >12 months), lack of sun exposure, malabsorption, chronic disease (liver/renal), drugs (anticonvulsants) and hereditary syndromes

63
Q

Presentation of rickets?

A 
FTT/short stature
Bowed legs
Hypoglycaemia (infants) - tetany/seizures
Harrisons sulcus
Frontal bossing
Expansion of metaphyses (esp. wrists)
64
Q

Investigations for rickets?

A

Diet diary/Hx

Bloods:
Serum calcium and albumin (low or normal)
phosphorous 
PTH (usually elevated)
ALP (+++)
LFTs and U+Es to exclude pathology

X-ray - wrists show widened epiphyses

65
Q

Hirsutism causes?

A 
PCOS
Cushing's
Congenital adrenal hyperplasia
Obesity (over conversion of oestrogens to androgens)
Adrenal tumour
androgen secreting ovarian tumour
Phenytoin

Paediatrics (14 decks)

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