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Paediatrics > Oncology, Neurology > Flashcards

Oncology, Neurology Flashcards

1
Q

How is childhood cancer classified?

A

ICCC (International classification of childhood cancer)

Based on tumour morphology (cell origin) and primary site

Standard classification is essential for comparing incidence & survival across regions & time periods

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2
Q

When are children more likely to get cancer?

A

At a younger age (0-4yo)

15-24 yo = another peak as they have an increased risk of germ cell tumours and lymphomas

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3
Q

In 10% what are possible causes that may be identified for cancer?

A
  • Genes (Down, Fanconi, BWS, Li-Fraumeni familial cancer syndrome, neurofibromatosis)
  • Environment (radiation, infection(e.g. EBV))
  • Iatrogenic (RT, chemo)
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4
Q

Is child cancer sporadic?

A

Usually yes but it is important to ask about risk factors

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5
Q

What makes the categories for referral in child cancer?

A

IMMEDIATE=unexplained petechiae, hepatosplenomegaly

URGENT=repeated attendance, same problem, no clear diagnosis OR new neuro symptoms, abdo mass

REFER (to doctor or for urgent investigation)=rest pain, back pain & unexplained lump, lymphadenopathy

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6
Q

What are some examples of oncological emergencies?

A
  • Sepsis/febrile neutropenia
  • Raised ICP
  • Spinal cord compression
  • Mediastinal mass
  • Tumour lysis syndrome
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7
Q

What are risks for sepsis/febrile neutropenia?

A

ANC< 0.5 x10 to the 9
Indwelling catheter
Mucosal inflam
High dose chemo/SCT

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8
Q

How do those with sepsis/febrile neutropenia present?

A
  • Fever (or low temp)
  • Rigors
  • Drowsiness
  • Shock (metabolic acidosis)

If child is not responding to simple measures and has significant shock sometimes they need ionotropic support to help their BP, transferred to PICU

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9
Q

What is the early presentation of raised ICP?

A
  • Early morning headache/vomiting
  • Tense fontanelle
  • Increasing HC (head circumference)
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10
Q

What are the signs of late presentation of raised ICP?

A
  • Constant headache
  • Papilloedema
  • Diplopia (VI palsy)
  • Loss of upgaze
  • Neck stiffness
  • Status epilepticus
  • Reduced GCS
  • Cushing’s triad (low HR, high BP, falling RR)
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11
Q

What is the investigation for raised ICP?

A

Imaging mandatory if safe

CT is good for screening

MRI is best for more accurate diagnosis

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12
Q

What is the management of raised ICP?

A

DEXAMETHASONE if due to tumour (reduce oedema & increase CSF flow)

NEUROSURGERY-urgent CSF diversion
- Ventriculostomy-hole in membrane at base of 3rd ventricle with endoscope
- EVD (temporary)
- VP shunt

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13
Q

In whom is spinal cord compression more common (potential complication of nearly all paed malignancies)?

A

Ewing’s or Medulloblastoma

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14
Q

When does spinal cord compression arise and what is the pathological process of it?

A

Diagnosis of cancer(65%), relapse, progression

  • Invasion from paravertebral disease via intervertebral foramina (40% extradural)
  • Vertebral body compression (30%)
  • CSF seeding
  • Direct invasion
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15
Q

What is the presentation of spinal cord compression?

A

Symptoms vary with level

  • WEAKNESS
  • PAIN
  • SENSORY
  • SPHINCTER DISTURBANCE
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16
Q

How is spinal cord compression managed?

A
  • URGENT MRI
  • Start DEXAMETHASONE urgently to reduce peri-tumour oedema
  • Definitive treatment with chemo is appropriate when rapid response is expected (surgery or RT are other options)
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17
Q

What does the outcome of spinal cord compression depend on?

A
  • Severity of impairment rather than the duration between symptoms and diagnosis

(Mild impairment >90% recovery, Paraplegic 65% recovery)

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18
Q

SVC syndrome (or SMS) is rare (<1% of new paediatric malignancies): what are the common causes of it?

A
  • LYMPHOMA
  • Other=neuroblastoma, germ cell tumour, thrombosis
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19
Q

How does SVC syndrome and SMS present and how is it investigated?

A

SVCS: facial, neck and upper thoracic plethora, oedema, cyanosis, distended veins, ill, anxious, reduced GCS

SMS: dyspnoea, tachypnoea, cough, wheeze, stridor, orthopnoea

Investigation:
CXR / CT chest (if able to tolerate)
Echo

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20
Q

What is the management of SVCS and SMS?

A

Keep upright & calm
Urgent biopsy (ideally)

Look to obtain important diagnostic information without GA
FBC, BM, pleural aspirate, GCT markers

Definitive treatment is required urgently:
- Chemotherapy is usually rapidly effective
- Presumptive treatment may be needed in the absence of a definitive histological diagnosis (steroids)

  • RT is effective (May cause initial increased respiratory distress)
  • Rarely surgery if insensitive
  • CVAD-associated thrombosis should be treated by thrombolytic therapy

Most of underlying malignancies have a good prognosis

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21
Q

What is tumour lysis syndrome caused by?

A

Metabolic derangement

Rapid death of Tumour Cells

Release of intracellular contents

At or shortly after presentation

Secondary to treatment

(rarely spontaneous)

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22
Q

What are the clinical features of tumour lysis syndrome?

A

INCREASED potassium, urate-relatively insoluble, phosphate

REDUCED calcium

Acute renal failure:
Urate load
CaPO4 deposition in renal tubules

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23
Q

What is the treatment of tumour lysis syndrome?

A

Avoidance
ECG Monitoring
Hyperhydrate-2.5l/m2
QDS electrolytes
Diuresis

NEVER GIVE POTTASIUM (or phosphate)

Decrease uric acid:
- Urate Oxidase-uricozyme (rasburicase)-acute setting
- Allopurinol

Treat hyperkalaemia:
Ca Resonium
Salbutamol
Insulin

Renal replacement therapy

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24
Q

What do oncologists use to see what cancer is and what harm it is causing?

A
  • Scans
  • Biopsy/pathology
  • Cytogenetics
  • Tumour markers
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25
Q

What tumours can secrete AFP?

A

Liver tumours or germ cell tumours

Can be diagnostic

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26
Q

How is cancer staged?

A

Staging-e.g. scans, bone marrow

CXR or CT chest

Bone scan

Number of different tests depending on what’s the primary tumour and the location of the primary tumour

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27
Q

What is cannonball metastases in the chest typical of?

A

Sarcoma diagnosis-indicate very poor prognosis

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28
Q

What does treatment of cancer depend on?

A

Multimodal therapy based on specific disease and extent (plus patient factors)

MDT approach

National/international collaboration

Clinical research

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29
Q

How does a bone marrow transplant work?

A

Collect STEM cells from somebody else and put
them back into a new patient where they will travel to the bone marrow and then set up a completely new immune system.

Bone marrow transplants allow you to use very high dose chemotherapy but they also give you an immune response where the donor immune system will recognise the host cancer cells as foreign and kill them using the same kind of approach as immunotherapy.

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30
Q

What are the acute risks of chemo?

A

Hair loss
Nausea & vomiting
Mucositis
Diarrhoea / constipation
Bone marrow suppression – anaemia, bleeding, infection

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31
Q

What are the chronic risks of chemo?

A

Organ impairment – kidneys, heart, nerves, ears

Reduced fertility

Second cancer

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32
Q

What are the acute and chronic risks of RT?

A

Acute:
Lethargy
Skin irritation
Swelling
Organ inflammation – bowel, lungs

Chronic:
Fibrosis / scarring
Second cancer
Reduced fertility

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33
Q

Survivors of childhood cancer have … toxicity

A

ACCUMULATIVE

(from being treated with childhood cancer)

34
Q

How so is child neurology dynamic?

A

Brain continues to grow and brain functions evolve

Neurodevelopment continues to progress

Static lesion produce evolving features

35
Q

Why is time course of symptoms crucial in a neurological condition?

A

To ascertain symptom progression - and to try to determine a differential diagnosis

Distinguishing static from slowly progressive symptoms can be challenging

36
Q

What is crucial to ask in a developmental Hx?

A
  • Motor milestones (gross and fine motor skills)
  • Speech and language development
  • Play esp symbolic play and social behaviour
  • Self help skills
  • Vision and hearing assessment

Global delay=if delayed in 2 or mote of these domains

Disordered development=1 of these fields

37
Q

What is included in the neurological examination in childhood?

A
  • Opportunistic approach and observation skills
  • Appearance
  • Gait
  • Head size
  • Skin findings (neurocutaneous markers (e.g. Cafe au lait spots—neurofibromatosis, Port wine stain—Sturge Weber syndrome)
38
Q

What neurological conditions are seen (examples)?

A

Migraine

Traumatic brain injury

Tourette syndrome (1% of all children with high frequency in ADHD & OCD)

Epilepsy

Brain tumours (2nd most common cancer in children)

39
Q

What are the categories of headache a child can have?

A
  • Isolated acute
  • Recurrent acute
  • Chronic progressive
  • Chronic non-progressive
40
Q

How would you classify a chronic headache?

A

Patient suffers from a sore head for at least 15 days out of 30 days in a month

41
Q

What should be included in a recurrent or chronic headache Hx?

A
  • Is there more than 1 type of headache

Typical episode
- Any warning
- Location
- Severity
- Duration
- Frequency

42
Q

What should be included in a headache examination?

A
  • Growth parameters, OFC, BP (HT can be a signal of intracranial pathology but can also itself cause headaches)
  • Sinuses, teeth, visual acuity
  • Fundoscopy
  • Visual fields (craniopharyngioma)
  • Cranial bruit
  • Focal neurological signs
  • Cognitive and emotional status

The diagnosis of headache etiology is clinical

43
Q

What pointers would point you towards childhood migraine?

A

Hemicranial pain - throbbing/pulsatile

Associated abdominal pain, nausea, vomiting

Focal symptoms/ signs before, during, after attack: Visual disturbance, paraesthesia, weakness (AURA)

‘Pallor’

Aggravated by bright light/ noise (Photophobia/phonophobia)

Relation to fatigue/ stress

Helped by sleep/ rest/ dark, quiet room

Family history often positive

44
Q

What pointers would make you think of a tension headache (as apposed to migraine)?

A
  • Diffuse, symmetrical
  • Band like distribution
  • Present most of the time (but there may be symptom free periods)
  • ‘constant headache’
45
Q

Pointers to raised ICP (Red flags)?

A

Aggravated by activities that raise ICP eg. Coughing, straining at stool, bending

Woken from sleep with headache +/- vomiting

46
Q

What presentation features would make you think of analgesic overuse headaches?

A

Headache is back before allowed to use another dose

Paracetamol/ NSAIDs

Particular problem with compound analgesics eg. Cocodamol

47
Q

In headache what are the indications for neuroimaging?

A

Features of cerebellar dysfunction

Features of raised ICP

New focal neurological deficit eg. new squint

Seizures, esp focal

Personality change

Unexplained deterioration of school work

48
Q

How is migraine managed (Acute & Preventative)?

A

Acute attack: effective pain relief, triptans

Preventative (at least 1/week): Pizotifen, Propranolol, Amitryptyline, Topiramate, Valproate

49
Q

How is TTH managed?

A

Aim at reassurance: no sinister cause

Attention to underlying chronic physical, psychological or emotional problems

Acute attacks: simple analgesia

Prevention: Amitryptiline

Discourage analgesics in chronic TTH

50
Q

What is the difference between a seizure/fit, syncope and convulsion and an epileptic seizure (all paroxysmal events)?

A

Seizure/ Fit: Any sudden attack from whatever cause

Syncope: Faint (a neuro-cardiogenic mechanism)

Convulsion: Seizure where there is prominent motor activity

Epileptic seizure: an electrical phenomenon

Seizures can have different mechanisms

Many seizures are not epileptic in nature

51
Q

What is an epileptic seizure and what does it depend on?

A

Epileptic seizure=An abnormal excessive hyper synchronous discharge from a group of (cortical) neurons

It may have clinical manifestations

Paroxysmal change in motor, sensory or cognitive function

Depends on seizure’s location, degree of anatomical spread over cortex, duration

52
Q

What is epilepsy?

A

Epilepsy: A tendency to recurrent, unprovoked (spontaneous) epileptic seizures

A question that must be answered clinically, with recourse to EEG only for supportive evidence

53
Q

Is a seizure always epilepsy?

A

NOOOOO

A seizure is not necessarily epileptic

Consequences of misdiagnosis of epilepsy can be serious

54
Q

What are some examples of non epileptic seizures and other mimics in children?

A

Acute symptomatic seizures: due to acute insults eg. Hypoxia-ischaemia, hypoglycemia, infection, trauma

Reflex anoxic seizure: common in toddlers (vagal overstimulation-provoked/triggered)

Syncope

Parasomnias eg. night terrors

Behavioural stereotypies (repetitive movements)

Psychogenic non-epileptic seizures (PNES)

55
Q

What is a febrile convulsion?

A

An seizure occurring in infancy/ childhood, usually between 3 months and 5 years of age, associated with fever but without evidence of intracranial infection or defined cause for the seizure

Commonest cause of ‘acute symptomatic seizure’ in childhood

56
Q

What are the seizure types (can be challenging to distinguish between)?

A

Jerk/ shake: clonic, myoclonic, spasms

Stiff: usually a tonic seizure

Fall: Atonic/ tonic/ myoclonic

Vacant attack: absence, focal absence seizure

57
Q

What is the mechanism of an epileptic fit?

A

Chemically triggered by chemical imbalance:
- Decreased inhibition (gama-amino-butyric acid, GABA)
- Excessive excitation (glutamate and aspartate)
- Excessive influx of Na and Ca ions

Chemical stimulation produces an electrical current

Summation of a multitude of electrical potentials results in depolarization of many neurons which can lead to seizures, can be recorded from surface electrodes (Electroencephalogram (EEG))

58
Q

What are the main two types of epileptic seizures?

A

Generalised seizure (neurons recruited from both halves of the brain)

Partial/focal seizure (restricted to one hemisphere or part of one hemisphere)

59
Q

What is the difference between childhood vs adult onset epilepsies?

A

Majority are idiopathic in origin (both Focal & Generalised)

Majority of epilepsies are generalised

Seizures can be subtle (absences, myoclonus, drop attacks)

Diagnosis can be challenging because:
- Non-epileptic paroxysmal disorders are more common in children
- Difficulty in explaining (Children are not young adults)
- Difficulty in interpretation (witness)
- Difficulty in interpretation and synthesising information(physician)

60
Q

What is the stepwise approach to a diagnosis of epilepsy?

A

Is the paroxysmal event epileptic in nature?

Is it epilepsy?

What seizure types are occurring?

What is the epilepsy syndrome?

What is the etiology?

What are the social and educational effects on the child?

61
Q

How is an EEG valuable in epilepsy and how is it not?

A

An interictal EEG has limited value in deciding when the individual has epilepsy

Sensitivity of first routine interictal EEG: 30- 60%

Problematic false positive rates: paroxysmal activity seen in 30%, frankly epileptiform activity in 5% of normal children

Useful in identifying seizure types, seizure syndrome and etiology

62
Q

How is epilepsy diagnosed?

A
  • History (before, during and after event)
  • Video recording of event
  • ECG in convulsive seizures (rule out long QT syndrome)
  • Interictal/ ictal EEG

MRI Brain: to determine etiology eg. Brain malformations/ brain damage

Genetics: idiopathic epilepsies are mostly familial; also single gene disorders eg. Tuberous sclerosis

Metabolic tests: esp if associated with developmental delay/ regression

63
Q

What is the management of epilepsies in children?

A

Anti-epileptic drugs (AED) should only be considered if diagnosis is clear even if this means delaying treatment

Role of AED is to control seizures, not cure the epilepsy

  • Start with one AED: slow upward titration until side-effects manifest or drug is considered to be inefficient.

Age, gender, type of seizures and epilepsy should be considered in selecting AEDs

S/Es: CNS related can be detrimental; Drowsiness, effect on learning, cognition and behavioural

64
Q

What drug treatment is available for epilepsy management?

A

Sodium Valproate (not in girls- recent MHRA advice) or Levetiracetam: first line for generalised epilepsies

Carbamazepine: first line for focal epilepsies

Several new AEDs with more tolerability and fewer side effects: Levatiracetam, Lamotrigine, Perampanel

Other therapies: steroids, immunoglobulins and ketogenic diet (mostly for drug-resistant epilepsies)

65
Q

What are some more management strategies for epilepsy (usually for drug resistant epilepsies)?

A

VNS (palliative-lessen burden of seizures on every day life)

SURGERY (palliative or curative-localise origin & may facilitate a resection)

66
Q

Assessing a child with an unusual head, why is this important?

A

Accurate measurements & interpretation as part of a childhood physical exam

Head size problems=Macrocephaly & microcephaly

Head shape problems-What not to miss

Refer early for specialist opinion

67
Q

In what order do the fontanelles close?

A

At birth, the bones of the infant skull are not fused together

Posterior fontanelle usually closes 2-3 months after birth

Followed by gradual fusion of the sutures

Anterior fontanelle usually closes between 1-3 years of age (average=18 months)

68
Q

What measurements should be done in terms of head circumference and in who should they be done?

A

Occipitofrontal circumference

As routine: Between birth- 3 years

In any child with neurological symptoms or developmental complaints

Measure and plot parental head sizes
Too big, too small or odd shape?
Sutures & Fontanelles?
Look at the facial features- any asymetry?

69
Q

What is microcephaly and what does it usually indicate?

A

Definition: OFC <2 SD: mild
OFC <3 SD: moderate/ severe

Microcephaly usually indicates small brain: ‘micranencephaly’

Prenatal or postnatal onset: is it crossing centiles downwards?
Timing of onset may be a clue
Multiple causes: antenatal, postnatal, genetic and environmental

70
Q

What is MACROcephaly and what should be considered?

A

Definition: OFC > 2SD

Is it crossing centiles upwards?- indicates that either the underlying brain or the underlying CSF is expanding in a way it shouldn’t

Sutures?-separation
Fontanelles?-very large
Familial?
Hydrocephalus?
Large brain?
Development normal?
Other physical abnormalities – facial features, hepatosplenomegaly, bony deformities etc

71
Q

Head shape problems usually in first year of life: what should be asked and what are the types of head shape problems to be aware of?

A

Timing of onset?
Is it getting better or worse?

Plagiocephaly ‘flat-head’
Brachycephaly ‘short head or flat at back’
Scaphocephaly ‘boat shaped skull’
Craniosynostosis (premature fusion of the cranial sutures)

72
Q

What is one of the commonest head shape problems

A

Deformational plagiocephaly

  • Due to position child is in
  • Parallelogram shape skull
73
Q

What is craniosynostosis?

A

Premature fusion of one or more sutures

Depending on which suture closed too early you may get some classical characteristic shapes which may indicate the type of synostosis is

74
Q

How is craniosynostosis usually assessed?

A

Either cranial CT scans or occasionally skull x-rays

75
Q

What would make you suspect a NM disorder?

A
  • Baby ‘floppy’ from birth
  • Slips from hands
  • Paucity of limb movements
  • Alert, but less motor activity
  • Delayed motor milestones
  • Able to walk but frequent falls
76
Q

What does the Gowers sign indicate?

A

Weakness around the pelvic girdle and lower limb muscles in particular

Prominent clinical sign which may indicate an underlying muscle condition (e.g. Muscular dystrophy)

77
Q

What is the most common muscular dystrophy occurring in childhood?

A

Duchenne muscular dystrophy

1/3500 male infants

78
Q

What gene is affected in DMD and what are the signs of this condition?

A

Xp21, dystrophin gene, 1/3500 male infants

Delayed gross motor skills

Symmetrical proximal weakness
- Waddling gait, calf hypertrophy
- Gower’s sign positive

Elevated Creatinine Kinase levels = >1000 in DMD

Cardiomyopathy

Respiratory involvement in teens

79
Q

Pes cavus (high arch feet) is a classic sign seen in what?

A

Some types of hereditary motor sensory neuropathies (typified by the charcot marie tooth disease)

80
Q

What is the anatomical approach to neuromuscular conditions to determine where is the sight of the lesion and what is the lesion?

A

Muscle: muscular dystrophies, myopathies- congenital and inflammatory, myotonic syndromes

Neuromuscular junction: myasthenic syndromes

Nerve: Hereditary or acquired neuropathies

Anterior Horn Cell: Spinal muscular atrophy

Paediatrics (17 decks)

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