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My Phase 3a Revision > PAEDS - NEURO / ENT / OPHTHALMOLOGY > Flashcards

PAEDS - NEURO / ENT / OPHTHALMOLOGY Flashcards

1
Q

CEREBRAL PALSY
What is cerebral palsy?
How does it progress?

A
  • Permanent disorder of movement + posture due to a non-progressive lesion of motor pathways in the developing brain
  • Sx develop over time as the brain starts to develop
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2
Q

CEREBRAL PALSY
What are the causes of cerebral palsy?

A
  • Antenatal (80%) = genetics, congenital malformations or infections
  • Intrapartum (10%) = hypoxic-ischaemic injury
  • Postnatal (10%) = IV haemorrhage (prems), meningitis/encephalitis, trauma (NAI), hydrocephalus, kernicterus
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3
Q

CEREBRAL PALSY
What are some early features of cerebral palsy?

A
  • Abnormal limb/trunk tone + posture with delayed motor milestones
  • Feeding issues > oromotor incoordination, slow feeding, gagging + vomiting
  • Abnormal gait when walking achieved
  • Hand preference before 12m + primitive reflexes after 6m
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4
Q

CEREBRAL PALSY
What are some non-motor presentations of cerebral palsy?

A
  • LDs, epilepsy, squints + hearing impairment
  • Joint contractures, hip subluxation + scoliosis
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5
Q

CEREBRAL PALSY
What are the 4 broad types of cerebral palsy?

A
  • Spastic (pyramidal, 70%)
  • Ataxic (10%)
  • Dyskinetic (athetoid, 10%)
  • Mixed (10%)
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6
Q

CEREBRAL PALSY
What is affected in spastic cerebral palsy?

A
  • UMN pathways damaged (pyramidal or corticospinal) so UMN signs
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7
Q

CEREBRAL PALSY
What are the main features of spastic cerebral palsy?

A
  • Limb tone persistently increased (spasticity, velocity-dependent)
  • Brisk deep tendon reflexes + extensor plantars (+ve Babinski)
  • Increased limb tone may suddenly yield under pressure (clasp knife)
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8
Q

CEREBRAL PALSY
What is spastic quadriplegic cerebral palsy?

A
  • All 4 limbs, trunk involved with tendency to opisthotonus (extensor posturing), poor head control + low central tone
  • More severe > associated with seizures, microcephaly, low IQ
  • May have Hx of HIE
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9
Q

CEREBRAL PALSY
What are the 3 subtypes of spastic cerebral palsy?

A
  • Hemiplegic
  • Quadriplegic
  • Diplegic
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10
Q

CEREBRAL PALSY
What is spastic hemiplegic cerebral palsy?

A
  • Unilateral involvement of arm + leg (arm worse)
  • Face spared, fisting of affected hand, flexed arm, tip-toe walking
  • Presents 4–12m, normal birth with no HIE
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11
Q

CEREBRAL PALSY
What is spastic diplegic cerebral palsy?

A
  • All 4 limbs (legs worse)
  • Hand function may be relatively normal but walking abnormal
  • Linked with preterm birth (periventricular brain damage)
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12
Q

CEREBRAL PALSY
What is ataxic cerebral palsy?

A
  • Cerebellum affected > cerebellar signs
  • Early trunk + limb hypotonia (symmetrical)
  • Poor balance + delayed motor development
  • Incoordination, ataxic gait + intention tremor
  • Mostly genetics, can be acquired brain injury
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13
Q

CEREBRAL PALSY
What is dyskinetic cerebral palsy?

A
  • Intellect unimpaired as basal ganglia affected (extra-pyramidal)
  • Associated with kernicterus + HIE
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14
Q

CEREBRAL PALSY
What are the features of dyskinetic cerebral palsy?

A
  • Intellect unimpaired as basal ganglia affected (extra-pyramidal)
  • Chorea, athetosis, dystonia
  • Muscle tone is variable (floppiness), involuntary movements, poor trunk control
  • Associated with kernicterus + HIE
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15
Q

CEREBRAL PALSY
What is meant by chorea?

A

Irregular, sudden + brief non-repetitive movements

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16
Q

CEREBRAL PALSY
What is meant by athetosis?

A

Slowly writhing movements distally like fanning fingers

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17
Q

CEREBRAL PALSY
What is meant by dystonia?

A

Twisting appearance from simultaneous contraction of agonist + antagonist muscles

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18
Q

CEREBRAL PALSY
What are the investigations of cerebral palsy?

A
  • Clinical Dx (assess posture, pattern of tone, hand function + gait)
  • Functional ability judged by Gross Motor Function Classification System
  • MRI head to identify cause but not necessary for Dx
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19
Q

CEREBRAL PALSY
What are the stages of the Gross Motor Function Classification System?

A
  • I = walks without limitation
  • II = with limitation
  • III = handheld mobility device
  • IV = III with limitation
  • V = wheelchair
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20
Q

CEREBRAL PALSY
What is the MDT approach of cerebral palsy?

A
  • Drs
  • Physio (tone + posture issues)
  • SALT (swallowing issues)
  • OT (home adjustments, help with ADLs)
  • School (special educational needs)
  • Social workers (benefits)
  • Dietitians (?PEG feeding)
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21
Q

CEREBRAL PALSY
What is the management of spasticity in cerebral palsy?

A
  • PO or IT baclofen
  • PO diazepam
  • Botox injection
  • Orthopaedic surgery
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22
Q

VISION
What is vision like in children?

A
  • Visual acuity is poor in the newborn but increases to adult levels by age 4
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23
Q

VISION
What are some causes of severe visual impairment?

A

Genetic –

  • Congenital cataracts
  • Albinism
  • Retinal dystrophy
  • Retinoblastoma
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24
Q

VISION
How might visual impairments present in children?

A
  • Loss of red reflex (i.e. cataract)
  • White reflex in pupil (retinoblastoma, cataract, retinopathy of prematurity)
  • Not smiling responsively by 6w
  • Lack of eye contact with parents
  • Random eye movements
  • Failure to fix + follow
  • Nystagmus, squint, photophobia
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25
Q

VISION
When is vision screened in children?

A
  • Pre-school + school entry
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26
Q

STRABISMUS
What is strabismus?
Is it normal?

A
  • Misalignment of visual axis (squint)
    • Transient neonatal misalignments common in first few months when looking at near objects, reduce by 2m, gone by 12w
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27
Q

STRABISMUS
What are the 2 divisions of strabismus?

A
  • Concomitant (non-paralytic, common) = often refractive error, differences in control of extra-ocular muscles
  • Paralytic (rare) = paralysis in ≥1 of the extra-ocular muscles (if rapid onset may be sinister SOL)
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28
Q

STRABISMUS
What is the difference between a manifest and latent strabismus?

A
  • Manifest = present when views a target binocularly
  • Latent = binocular vision interrupted
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29
Q

STRABISMUS
What are the different types of manifest strabismus?
How does this compare to latent strabismus?

A
  • Esotropia = inward moving (cross-eyed)
  • Exotropia = outward moving
  • Hypertropia = upward moving
  • Hypotropia = downward moving
  • Latent is same but -phoria not -tropia (esophoria etc)
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30
Q

STRABISMUS
What is the pathophysiology of strabismus?

A
  • When eyes not aligned the images on retina do not match + pt will experience diplopia
  • When this occurs in paeds, before the eyes have fully established their connections within the brain, the brain will cope by reducing the signal from the less dominant eye
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31
Q

STRABISMUS
What is a complication of strabismus?

A
  • One eye used to see (dominant) + one eye ignored (lazy)
  • If untreated lazy eye becomes progressively more disconnected from brain over time + problem worsens (amblyopia)
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32
Q

STRABISMUS
What causes strabismus?

A
  • Multifactorial (combination of hereditary + refractive errors)
  • Idiopathic
  • Secondary to vision loss
  • Higher incidence in cerebral palsy
  • SOL (retinoblastoma) rare but suspect if sudden onset + other neurology
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33
Q

STRABISMUS
What are 3 types of refractive errors?

A
  • Hypermetropia = long-sightedness (common, hard to see nearby objects)
  • Myopia = short-sightedness (uncommon, less likely to cause permanent visual damage)
  • Amblyopia = defective visual acuity that persists after correction of refractive error + removal of any pathology (lazy eye)
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34
Q

STRABISMUS
How does amblyopia present?

A
  • Often unilateral, potentially permanent loss of visual acuity in an eye that has not received a clear image
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35
Q

STRABISMUS
What are some causes of amblyopia?

A

Any interference with visual development > squint, refractive error, ptosis, cataracts

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36
Q

STRABISMUS
What are some investigations for strabismus?

A
  • (Single) cover test for manifest/tropias
  • Cover-uncover (alternate cover) test for latent/phorias
  • Corneal light reflex test (Hirschberg’s test)
  • Important to assess visual acuity + ocular movements to exclude paralytic
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37
Q

STRABISMUS
Explain the cover test

A
  • Cover eye + observe the other eye for a shift in fixation
  • Direction of shift indicates the type of tropia
  • Close (33cm) + distant (6m) as some squints only present at one distance
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38
Q

STRABISMUS
Explain the cover-uncover test

A
  • Helps determine if misalignment is a tropia or phoria
  • Occlude eye + then quickly uncover, observing the occluded eye for refixation movement
  • A phoria will shift back to being straight, direction is opposite to the movement (shifts lateral = esophoria)
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39
Q

STRABISMUS
Explain the corneal light reflex test

A
  • Shine a pen torch in the eyes
  • Reflection of light should appear in the same position in both eyes
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40
Q

STRABISMUS
What is the management of amblyopia?

A
  • Early Tx = better to avoid damage, <7y ideal
  • Refractive adaptation = wear appropriate glasses for 16-18w
  • Occlusion of ‘good’ eye (part/full time) to force weaker eye to develop
  • Atropine drops in better eye causing vision in that eye to be blurred
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41
Q

STRABISMUS
What are the aims of strabismus management?

A
  • Restore comfortable binocular single vision
  • Eliminate diplopia
  • Restore good alignment of the eyes
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42
Q

STRABISMUS
What are some conservative techniques for strabismus?

A
  • Glasses/contact lenses
  • Prisms for diplopia
  • Orthoptic exercises to improve control over eye muscles
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43
Q

STRABISMUS
What medical treatment can be given in strabismus?

A
  • Botox injections = paralyse the muscle that is pulling the eye in a certain direction
  • Esotropia = MR, exotropia = LR
  • May need repeat injections as effects wear off, ketamine anaesthesia
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44
Q

STRABISMUS
What surgery may be offered in strabismus?

A
  • Strengthening procedure = resection of muscle on side eye does not face
  • Weakening procedure = recession of muscle on side the eye goes towards
  • Esotropia = bilateral MR recession or MR recession + LR resection
  • Exotropia = bilateral LR recession or LR recession + MR resection
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45
Q

HEARING
What are the 3 types of hearing loss?

A
  • Sensorineural = nerve damage (progressive, never reversible)
  • Conductive = obstruction in ear canal which prevents sound from getting through, bone conduction can still transmit sound (often reversible)
  • Mixed
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46
Q

HEARING
What are some causes of conductive hearing loss?

A
  • # 1 = congestion behind eardrums (viral URTI)
  • Glue ear, ear wax, middle ear infection, perforated ear drum
  • Structural abnormality of the outer ear (syndromes)
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47
Q

HEARING
What are some causes of sensorineural hearing loss?

A
  • Genetic or syndromes
  • Perinatal (trauma, infection, hypoxia)
  • Congenital infections (rubella, CMV)
  • Meningitis (pneumococcus can cause ossification of cochlear)
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48
Q

HEARING
What are some risk factors for conductive hearing loss?

A
  • Down’s syndrome,
  • craniofacial syndromes
  • cleft palate
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49
Q

HEARING
What are some risk factors for sensorineural hearing loss?

A
  • Premature,
  • FHx
  • consanguinity
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50
Q

HEARING
How might hearing loss present?

A
  • Parental concern
  • Incidental finding on screening
  • Problems with speech, behaviour or education (ignoring calls or sounds)
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51
Q

HEARING
What are some behavioural changes that might occur in hearing loss?

A
  • Sits near TV + volume loud
  • Misunderstands/slow in responding or answers incorrectly
  • Soft/fuzzy speech
  • Does not turn immediately when named called
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52
Q

HEARING
What 2 types of hearing tests are part of the newborn hearing screening programme (NHSP)?

A
  • Evoked otoacoustic emission (EOAE)
  • Auditory brainstem response (ABR) audiometry if EOAE fails
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53
Q

HEARING
What is evoked otoacoustic emission?
What are the pros?
What are the cons?

A
  • Earphone produces sound which evokes an echo from ear if cochlear function normal
  • Simple + quick
  • Misses auditory neuropathy, cochlear test not hearing, high false +ve in first 24h
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54
Q

HEARING
What is auditory brainstem response audiometry?
What are the pros?
What are the cons?

A
  • Computer analysis of EEG waveforms evoked in response to auditory stimuli
  • Screens hearing pathway ear>brainstem, low false +ve rate
  • Affected by movement (time consuming), electrodes on infant’s head, complex computerised gear
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55
Q

HEARING
What testing might be done in children 6–9m?

A
  • Distraction testing
  • Relies on baby locating + turning appropriately to high + low frequency sounds out of field of vision
  • 2x trained staff
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56
Q

HEARING
What testing might be done in children 10–18m?

A
  • Visual reinforcement audiometry
  • Hearing thresholds are established using visual rewards (illumination of toys) to reinforce the child’s head turn to stimuli of different frequencies
  • First test that does single ear measures
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57
Q

HEARING
What hearing tests are done at…

i) >2y?
ii) >2.5y?
iii) 4y?

A

i) Performance testing = child performs an action when hear a noise
ii) Speech discrimination tests (McCormick toy test)
iii) Pure tone audiometry at school entry = child responds to pure tone stimulus with headphones

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58
Q

HEARING
What are 3 main investigations in hearing?

A
  • Rinne’s test (mastoid then external acoustic meatus)
  • Weber’s (forehead in midline)
  • Audiograms
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59
Q

HEARING
What does Rinne’s test show you?

A
  • Normal = louder at EAM
  • Conductive = louder on mastoid
  • Sensorineural = both decreased
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60
Q

HEARING
What does Weber’s test show you?

A
  • Normal = vibrations equal in both ears
  • Conductive = louder in abnormal ear
  • Sensorineural = louder in normal ear
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61
Q

HEARING
What do audiograms show you?

A
  • Frequency (Hz, x) low>high + volume (dB, y) bottom = loud
  • Anything above 20dB line is normal
  • Sensorineural = both air + bone conduction impaired (>20dB)
  • Conductive = only air conduction impaired (>20dB), bone normal
  • Mixed = both impaired but air worse (>15dB difference)
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62
Q

HEARING
What are some complications of hearing issues?

A
  • Developmental delay (speech + language)
  • Social/behavioural problems (too loud or too quiet)
  • Impact on education, friendships/social life + psychologically
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63
Q

HEARING
What is the management of conductive hearing loss?

A
  • Most self-limiting so watch + wait
  • ENT referral for insertion of grommets to help drain excess fluid if necessary
  • Temporary hearing aids or if permanent cause
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64
Q

HEARING
What is the management of sensorineural hearing loss?

A
  • Hearing aids > aim to improve hearing so as much speech audible as possible
  • Cochlear implants reserved for profound hearing loss (>95dB), high frequency, bilateral hearing loss or meningitis related
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65
Q

HEARING
What is the management of mixed hearing loss?

A
  • Correct conductive problem first + then offer hearing aid
66
Q

DEVELOPMENT MDT
What is the child development service?

A
  • MDT + multi-agency (health, social services, education) with aim of providing coordinated service with good inter-agency liaison to meet the functional needs of the child
67
Q

DEVELOPMENT MDT
What is the role of child developmental services?

A
  • Liaise between home, school + the child’s care needs
  • Assess child’s functional ability + need
  • Provide therapy + psychosocial support where needed
  • Ensure health needs of child are met
68
Q

DEVELOPMENT MDT
Name some members of the child development services MDT and their role

A
  • Paediatrician = Ax, Ix + Dx, continuing medical Mx, coordination
  • Physio = balance + mobility, prevent contractures, mobility aids
  • OT = ADLs, house adaptations
  • SALT = feeding, speech + language development
  • Dietician = advice on nutrition
  • Social worker = benefits
  • Psychologist = cognitive testing, behaviour management
  • Specialist health visitor + key workers = coordinate MDT + multi-agency care
69
Q

SEIZURES
What is a seizure?

A
  • Sudden disturbance of neurological function due to excessive neuronal discharge
70
Q

SEIZURES
What are some causes of seizures?

A
  • Epilepsy
  • Febrile convulsions
  • Metabolic (hypoglycaemia, hypocalcaemia)
  • Head trauma, infection (meningitis, encephalitis)
  • Toxins, iatrogenic (post-brain surgery)
71
Q

FEBRILE CONVULSIONS
What is a febrile convulsion?

A
  • Seizures provoked by a fever in otherwise normal children
72
Q

FEBRILE CONVULSIONS
When does it happen?

A

Usually early in viral infections as temperature rises rapidly

73
Q

FEBRILE CONVULSIONS
What is the epidemiology?

A
  • 3% of children,
  • 6m–6y
  • often genetic predisposition
74
Q

FEBRILE CONVULSIONS
What are the 3 types?

A
  • Simple
  • complex
  • febrile status epilepticus
75
Q

FEBRILE CONVULSIONS
What is a simple febrile convulsion?

A
  • Generalised (tonic-clonic) seizure
  • <15m
  • Typically no recurrence within 24h
  • Recovery within 1h
76
Q

FEBRILE CONVULSIONS
What is a complex febrile convulsion?

A
  • Focal seizure
  • 15–30m
  • May recur within 24h
77
Q

FEBRILE CONVULSIONS
What is a febrile status epilepticus?

A

A complex febrile convulsion that lasts for over 30 minutes

78
Q

FEBRILE CONVULSIONS
What are some complications of febrile convulsions?

A
  • Usually no lasting damage
  • 1 in 3 will have another febrile convulsion
  • 2-7% will develop epilepsy after simple, 10–20% after complex
79
Q

FEBRILE CONVULSIONS
What is the management of febrile convulsions?

A
  • Period of observation, paeds referral if first seizure or complex
  • Antipyretics have NOT shown to reduce risk of recurrence
  • Education = stay with them, ensure safe, nothing in mouth, call 999 if lasts >5m, teach how to use PR diazepam or buccal midazolam if Hx of prolonged seizures (>5m)
80
Q

EPILEPSY
What is epilepsy?

A
  • Recurrent tendency to have unprovoked seizures
81
Q

EPILEPSY
What are the 2 phases?

A
  • Ictal = early phase w/ positive Sx such as excessive activity (jerky actions)
  • Post-ictal = later phase w/ negative Sx such as weakness, drowsiness
82
Q

EPILEPSY
What are some causes of epilepsy?

A
  • 2/3rd idiopathic, FHx, alcohol/drugs (+ withdrawal)
  • Brain injury (hypoxia, trauma, surgery)
  • SOL (tumour, abscess)
  • CNS infection (meningitis, encephalitis)
83
Q

EPILEPSY
What are the two different types of seizures?

A
  • Focal/partial seizures = arise from one area of cortex or part of one hemisphere
  • Generalised = discharge arises from both hemispheres
84
Q

EPILEPSY
What are the 3 types of partial seizures?

A
  • Simple-partial = consciousness + awareness
  • Complex-partial = without consciousness + awareness
  • Secondary generalised = seizures start in one hemisphere but then spread to both (focal>general)
85
Q

EPILEPSY
How would a partial seizure present in…

i) frontal lobe?
ii) temporal lobe?
iii) parietal lobe?
iv) occipital lobe?

A

i) Strange smells, motor movements, Jacksonian march
ii) Déjà/jamais-vu, automatisms (chewing, lip smacking), hallucinations, aura/sensations, amnesia
iii) Contralateral altered sensations (tingling, electric-shock)
iv) Flashing lights, eyelid fluttering, eye movements

86
Q

EPILEPSY
What is…

i) Jacksonian march?
ii) Todd’s paresis?

A

i) Motor twitch starts on one side of body then “marches” over a few seconds to affect larger parts of both like entire hand, foot + may generalise
ii) Focal weakness in a part or all of the body after a seizure

87
Q

EPILEPSY
What are the 4 main types of generalised seizures?

A
  • Absence seizures
  • Tonic-clonic seizures
  • Myoclonic seizures
  • Atonic (akinetic) seizures “drop attacks”
88
Q

EPILEPSY
What are absence seizures?

A

Brief (<30s) pauses where activity stops (still, silent, stares), may have slight eyelid flickering, can be precipitated by hyperventilation

89
Q

EPILEPSY
What is the epidemiology of absence seizures?

A
  • Onset 4-8y,
  • F>M,
  • may progress tonic-clonic later
90
Q

EPILEPSY
What are the investigations for absence seizures?

A

EEG = 3hz generalised spike, symmetrical

91
Q

EPILEPSY
What is the prognosis for absence seizures?

A

Good, 90% seizure free in adolescence

92
Q

EPILEPSY
What is a tonic-clonic seizure?

A
  • Tonic = vague warning, rigidity, falls + may make sound, LOC + can stop breathing
  • Clonic = convulsions, bilateral rhythmic muscle jerks, irregular breathing, may tongue bite (lateral) or urinary incontinence
  • Post-ictal = drowsy, confused, irritable or depressed
93
Q

EPILEPSY
What is a myoclonic seizure?

A
  • Brief, sudden muscle contractions like jerk of limb, face or trunk
  • Usually remains awake, can occur in juvenile myoclonic epilepsy
  • Can be physiological (hiccups, sleep myoclonus)
94
Q

EPILEPSY
What is an atonic (akinetic) seizure/drop attack?

A
  • Brief, sudden loss of muscle tone causing a fall but no LOC
  • Often begin in childhood, ?indicate Lennox-Gastaut syndrome
95
Q

EPILEPSY
What are 4 epilepsy syndromes seen in children?

A
  • Infantile spasms (West’s syndrome)
  • Lennox-Gastaut syndrome
  • Juvenile myoclonic epilepsy
  • Benign Rolandic epilepsy = M>F, paraesthesia (unilateral face, tongue, twitching) during sleep, EEG shows centrotemporal focal spike waves
96
Q

EPILEPSY
Who is affected by infantile spasms?

A
  • Early life (4-6m), M>F, often secondary to serious neuro abnormality (tuberous sclerosis, encephalitis, birth asphyxia)
97
Q

EPILEPSY
What is the management of infantile spasms?

A

Vigabatrin or corticosteroids (poor prognosis)

98
Q

EPILEPSY
What are the 3 components to infantile spasms?

A
  • Violent flexor spasms of head, trunk + limbs followed by extension of arms (salaam spasms) for 1-2s, can repeat up to 50 times
  • Progressive mental handicap
  • EEG shows hypsarrhythmia
99
Q

EPILEPSY
What is Lennox-Gastaut syndrome?
How does it present?
Management?

A
  • Can be extension of infantile spasms, 1-5y
  • Atypical absences, falls, jerks + 90% have mod-severe mental handicap
  • EEG shows slow spike, ketogenic diet may help
100
Q

EPILEPSY
Who is juvenile myoclonic epilepsy more common in?
How does it present?
Management?

A
  • Teens, F>M
  • Infrequent generalised seizures (often morning), daytime absences, sudden shock-like myoclonic seizures (can happen before seizures)
  • Good response to valproate
101
Q

EPILEPSY
What are some investigations for epilepsy?

A
  • Mostly clinical Dx + witness Hx crucial
  • Exclude organic causes with FBC, U+E, LFTs, glucose, ECG
  • EEG, often sleep deprived or hyperventilate to provoke
  • ?Neuroimaging (CT/MRI head) if focal neurology + concerns of SOL
102
Q

EPILEPSY
What is the general management of epilepsy?
What are the treatment principles?

A
  • Ensure little harm, maintain airway, do not restrain
  • Aim for monotherapy, maximum tolerated dose before changing or adding drugs, avoid abrupt withdrawal
103
Q

EPILEPSY
What is the management of generalised seizures?

A
  • 1st line = sodium valproate
  • 2nd line = lamotrigine, carbamazepine (TC), clonazepam (myoclonic)
104
Q

EPILEPSY
What is the management of myoclonic seizures?

A
  • 1st line = sodium valproate
  • 2nd line = clonazepam
105
Q

EPILEPSY
What is the management of focal seizures?

A
  • 1st line = carbamazepine or lamotrigine
  • 2nd line = levetiracetam or sodium valproate
106
Q

EPILEPSY
What is the management of absence seizures?

A
  • Ethosuximide or sodium valproate
107
Q

EPILEPSY
What is a note about treatment with carbamazepine?

A
  • Can exacerbate absent + myoclonic seizures
108
Q

EPILEPSY
What last line treatments may be used in epilepsy?

A
  • Vagal stimulation,
  • surgery (hemispherectomy, non-dominant lobectomy)
109
Q

‘FUNNY TURNS’
What are the triggers for reflex anoxic seizures?

A
  • Pain or discomfort,
  • cold food,
  • fright (emotions)
110
Q

‘FUNNY TURNS’
What are the causes of reflex anoxic seizures?

A

Cardiac asystole from vagal inhibition to heart (syncopal episode)

111
Q

‘FUNNY TURNS’
What is the clinical presentation of reflex anoxic seizures?

A
  • Child becomes pale + falls to floor,
  • hypoxia may induce generalised tonic-clonic seizure which is brief + child RAPIDLY recovers
112
Q

‘FUNNY TURNS’
What are the investigations for reflex anoxic seizures?

A
  • Ocular compression under controlled conditions often lead to asystole
  • paroxysmal slow-wave discharge on EEG
113
Q

‘FUNNY TURNS’
What are the triggers for breath holding attacks?

A

Upset, worked up or angry

114
Q

‘FUNNY TURNS’
What is the clinical presentation of breath holding attacks?

A
  • Child cries, holds their breath + goes cyanotic,
  • sometimes brief LOC but RAPID recovery
115
Q

‘FUNNY TURNS’
What are breath holding attacks associated with?

A

Linked with Fe anaemia so treating as such may minimise further ones

116
Q

‘FUNNY TURNS’
What are some other causes of ‘funny turns’?

A
  • Syncope
  • Migraine
  • Benign paroxysmal vertigo
  • Cardiac arrhythmias
  • NEAD
  • Fabricated by parent or child
117
Q

‘FUNNY TURNS’
What is the presentation of syncope?

A
  • Clonic movements may occur,
  • triggers like hot/stuffy,
  • standing long
118
Q

‘FUNNY TURNS’
What is the presentation of migraine?

A
  • Can happen ±headache,
  • unsteadiness/light headedness with other classic migraine Sx
119
Q

‘FUNNY TURNS’
What is the presentation of benign paroxysmal vertigo?

A
  • Nystagmus,
  • unsteady,
  • headache
120
Q

DISORDERS
Name 2 neurocutaneous disorders
What is the mode of inheritance for these conditions?

A
  • Neurofibromatosis (type 1 + 2) + tuberous sclerosis
  • AD
121
Q

NEUROFIBROMATOSIS
What is the clinical presentation of neurofibromatosis 1?

A
  • No intellectual problems but lots of skin involvement
  • > 5 café-au-lait spots
  • Axillary freckling in skin folds
  • Iris hamartomas, scoliosis + pheochromocytomas
  • Peripheral neurofibromas
122
Q

NEUROFIBROMATOSIS
What is the clinical presentation of neurofibromatosis 2?

A
  • Hearing problems with no skin involvement
  • Bilateral vestibular schwannomas > sensorineural hearing loss then tinnitus + vertigo
123
Q

TUBEROUS SCLEROSIS
What are the cutaneous features of tuberous sclerosis?

A
  • Hypopigmented ‘ash-leaf’ spots which fluoresce under UV light
  • Roughened (Shagreen) patches of skin over lumbar spine
  • Angiofibromas (butterfly distribution over nose)
  • Subungual fibromata
124
Q

TUBEROUS SCLEROSIS
What are some other features of tuberous sclerosis?

A
  • Neuro = epilepsy (infantile spasms or partial), developmental delay + intellectual impairment
  • Retinal hamartomas,
  • polycystic kidneys,
  • rhabdomyomata of heart
125
Q

TUBEROUS SCLEROSIS
What are the investigations?

A

CT/MRI will detect calcified subependymal nodules + tubers from 2nd year of life

126
Q

NEURAL TUBE DEFECTS
What are neural tube defects?

A
  • Failure of normal fusion of the neural plate to form neural tube during first 28d pregnancy
127
Q

NEURAL TUBE DEFECTS
What are the risk factors?

A

If you have a child with neural tube defect there is 10x increased risk of second foetus having similar problems

128
Q

NEURAL TUBE DEFECTS
What are neural tube defects associated with?

A
  • Insufficient folic acid
  • anti epileptic drugs
129
Q

NEURAL TUBE DEFECTS
What are 5 different types of neural tube defects?

A
  • Spina bifida occulta (#1)
  • Meningocele
  • Myelomeningocele (most severe)
  • Anencephaly
  • Encephalocele
130
Q

NEURAL TUBE DEFECTS
What is spina bifida occulta?

A
  • Failure of fusion of the vertebral arch, often incidental XR finding
131
Q

NEURAL TUBE DEFECTS
What is the presentation of spina bifida occulta?

A

Site may have identifiable birthmark, lipoma or hair patch (lumbar)

132
Q

NEURAL TUBE DEFECTS
What is the management of spina bifida occulta?

A

Neurosurgery

133
Q

NEURAL TUBE DEFECTS
What is meningocele?

A
  • Sac of fluid protruding spinal canal (without neural tissue), not exposed
134
Q

NEURAL TUBE DEFECTS
What is a myelomeningocele?

A
  • Sac of fluid protruding spinal canal (with neural tissue), open lesion
135
Q

NEURAL TUBE DEFECTS
How may a myelomeningocele present?

A
  • Paralysis of legs,
  • dislocation of hip + talipes,
  • sensory loss,
  • neuropathic bladder + bowel,
  • scoliosis
  • hydrocephalus from Chiari malformation
136
Q

NEURAL TUBE DEFECTS
How does Chiari malformation lead to hydrocephalus?

A
  • Herniation of cerebellar tonsils + brainstem > foramen magnum = disrupt CSF flow
137
Q

NEURAL TUBE DEFECTS
What is the management of myelomeningocele?

A
  • Close back lesion,
  • physio for paralysis,
  • ?indwelling catheter,
  • shunt
138
Q

NEURAL TUBE DEFECTS
What is anencephaly?

A
  • Failure to develop cranium + brain,
  • stillborn or die rapidly
139
Q

NEURAL TUBE DEFECTS
What is the management of anencephaly?

A

Antenatal USS Dx with TOP usually performed

140
Q

NEURAL TUBE DEFECTS
What is encephalocele?

A
  • Brain + meninges extrude through midline skull defect
141
Q

NEURAL TUBE DEFECTS
What is the management of encephalocele?

A
  • Surgical correction but often underlying cerebral malformations
142
Q

NEURAL TUBE DEFECTS
What can be used as prophylaxis for neural tube defects?

A
  • Folic acid (0.4mg for normal pregnancies, 5mg if high risk
143
Q

OTITIS MEDIA
What is otitis media?

A
  • Acute infection of middle ear, affects most children, common 6–12m
144
Q

OTITIS MEDIA
What are some causes of otitis media?

A
  • Viral (RSV, rhinovirus)
  • Bacterial - pneumococcus, Group A strep, H.Influenzae
145
Q

OTITIS MEDIA
What are some complications of otitis media?

A
  • Extracranial = mastoiditis, tympanic membrane perforation, glue ear
  • Intracranial = meningitis, abscess, venous sinus thrombosis
146
Q

OTITIS MEDIA
What is the management of otitis media?

A
  • Regular pain relief (paracetamol, ibuprofen)
  • Most resolve spontaneously, may need amoxicillin/co-amoxiclav
147
Q

OTITIS MEDIA
Who is most at risk?

A

Younger children as Eustachian tubes short, horizontal + function poorly

148
Q

OTITIS MEDIA
What is the clinical presentation of otitis media?

A

Ear pain, fever, reduced hearing ± coryza

149
Q

GLUE EAR
What is glue ear/otitis media with effusion (OME)?

A
  • Most common cause of conductive hearing loss in children
150
Q

GLUE EAR
What is the management?

A
  • Insertion of ventilation tubes (grommets) to drain excess fluid
  • Adenoidectomy as adenoids can harbour organisms + obstruct Eustachian tube so poor ventilation + drainage
151
Q

GLUE EAR
What investigations would you do?

A
  • Otoscopy (TM appears dull + retracted, often with visible fluid level)
  • Flat trace on tympanometry + evidence of conductive loss on pure tone audiometry (or reduced hearing on distraction test if younger)
152
Q

GROMMETS
what are grommets?

A

tiny tubes inserted into the tympanic membrane

they allow fluid to drain from the middle ear into the ear canal

153
Q

DEAFNESS
what are the different types of deafness?

A

sensorineural
conductive

154
Q

DEAFNESS
At what volume does deafness begin to cause problems with development?

A

hearing loss up to 20dB does not affect development

loss over 40dB affects speech and language development

155
Q

DEAFNESS
what are the causes of sensorineural hearing loss?

A

Inherited/genetic - ushers syndrome, Waardenburg syndrome

Acquired
- perinatal - birth asphyxia, hyperbilirubinemia, congenital infection (rubella, CMV, syphilis)
- postnatal - drugs, meningitis, head injury, labyrinthitis, acoustic neuroma

156
Q

DEAFNESS
what are the causes of conductive hearing loss?

A

External - ear canal atresia/stenosis

Middle ear - acute/chronic otitis media, glue ear

157
Q

PERIORBITAL CELLULITIS
what is it?

A

an infection of the eyelid or skin around the eye

158
Q

PERIORBITAL CELLULITIS
what is the clinical presentation?

A

Unilateral eyelid swelling and erythema
Unilateral eye pain/tenderness
Fever/malaise/irritability
Ptosis
Consider history of foreign body or traumatic eye injury

159
Q

PERIORBITAL CELLULITIS
what are the causes?

A
  • following minor injury to the eye
  • following another infection such as cough or cold
160
Q

PERIORBITAL CELLULITIS
what are the investigations?

A
  • assessment of eye movements
  • visual acuity
  • assessment of cranial nerves + pupillary responses
  • CT sinus and orbits with contrast medium
  • bloods - WBC, blood cultures
161
Q

PERIORBITAL CELLULITIS
what is the management?

A

Mild = oral co-amoxiclav/cefuroxime + metronidazole for 7-10 days
Moderate-severe = immediate referral to hospital + IV cefotaxime/clindamycin

can also consider incision, drainage and culture of any abscesses

162
Q

PERIORBITAL CELLULITIS
what are the complications?

A

can progress to orbital cellulitis - infection involves the deeper tissues around the eye and the eyeball itself

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