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PHASE 3A > PAEDS - opthalmology, ENT, derm/allergy, genetics > Flashcards

PAEDS - opthalmology, ENT, derm/allergy, genetics Flashcards

1
Q

what are the 2 types of squint in paeds? which is more common?

A
  1. concomitant squint - MORE COMMON, due to differences in the control of the extraocular muscles
  2. paralytic squint - due to paralysis in one or more of the extraocular muscles
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2
Q

causes of a squint

A

in otherwise healthy children - IDIOPATHIC

other:
- hydrocephalus
- cerebral palsy
- space-occupying lesion e.g. retinoblastoma
- trauma

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3
Q

why does a squint happen?

A
  1. eyes are misaligned
  2. images on retina won’t match and child experiences double vision
  3. brain copes by reducing signal from the less dominant eye
  4. results in one dominant eye and one lazy eye
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4
Q

what is ambylopia?

A

can happen if a squint isn’t fixed - lazy eye becomes progressively more disconnected from the brain and problem gets worse

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5
Q

investigations for a squint

A
  1. to detect squint - use Hirschberg’s test
  2. to identify nature of squint - Cover test
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6
Q

what is Hirschberg’s test and the cover test? what will the result be if the child has a squint?

A

Hirschberg’s - shine torch on patient’s eye, light will reflect asymmetrically on the pupils rather than symmetrically

Cover test - one eye covered, other eye focuses on object. cover is moved to the other eye and in a squint the noncovered eye will drift in or out

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7
Q

why is it important to manage a squint before the age of 8?

A

visual fields are still developing up to this age

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8
Q

management options for a squint

A

mainstay = occlusive patch over dominant eye

alternative = atropine drops in dominant eye (makes it blurry)

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9
Q

what is periorbital cellulitis? how does it differ from orbital cellulitis?

A

a superficial infection of the eyelid, anterior to the orbital septum. ocular function remains intact.

in orbital cellulitis, the muscle and fat within the orbit (posterior orbital septum) is infected

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10
Q

causes of periorbital cellulitis

A

normally a superficial tissue injury (chalazion, insect bite etc) or adjacent sinusitis

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11
Q

RFs for periorbital cellulitis (5)

A
  1. sinusitis infection
  2. young age
  3. male sex
  4. lack of Hib vaccine
  5. recent insect bite/stye etc
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12
Q

signs and symptoms of periorbital cellulitis

A
  • redness and swelling of eye
  • eyelid oedema
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13
Q

investigations and findings for periorbital cellulitis

A
  1. ophthalmological examination - no decreased vision but eyelid oedema and erythema seen
  2. bloods - elevated WBC
  3. CT sinus and orbits - inflammation of tissues anterior to orbital septum, LACK of orbital inflammation
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14
Q

management for mild periorbital cellulitis

A

PO cefalexin or cefuroxime

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15
Q

management for moderate periorbital cellulitis

A

IV flucloxacillin/ceftriaxone

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16
Q

investigations and management of severe periorbital cellulitis/orbital cellulitis?

A
  1. urgent opthal/ENT advice
  2. urgent CT scan (orbits, sinuses and brain)
  3. FBC, cultures, G&S +- LP

tx with 3rd gen cephalosporin + fluclox

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17
Q

what can periorbital cellulitis progress to?

A

orbital cellulitis - a medical emergency requiring hospital admission

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18
Q

complication of periorbital cellulitis

A

mastoiditis

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19
Q

how does mastoiditis present?

A
  • postauricular (behind ear) erythema and tenderness
  • fever
  • otalgia
  • otorrhoea (discharge)
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20
Q

how is mastoiditis investigated and managed?

A
  • need to do CT of mastoid bone and brain
  • needs IV abx and fluid resus if unstable, analgesia and antipyrexials
  • if complications, incision and drainage
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21
Q

what is glue ear?

A

a condition where viscous inflammatory fluid builds within the middle ear cavity, sometimes resulting in conductive hearing impairment

22
Q

epidemiology of glue ear

A

most common cause of transient deafness in children
8 out of 10 children will have it by age 10

23
Q

RFs for glue ear

A
  1. bottle fed
  2. household smoking
  3. atopy
  4. genetic disorders e.g mucociliary (like CF) or craniofacial (like Down’s syndrome)
24
Q

pathophysiology of glue ear

A
  1. eustachian tube (connects middle ear cavity to nasal cavity)
  2. ET is needed to equilibriate pressure within the middle ear with atmosphere
  3. ET more likely to get blocked in children as it’s shorter and more horizontal
  4. blocked ET = impaired middle ear ventilation
  5. mucosal cells lining middle ear cavity produce fluid due to negative pressure
  6. subsequent mucosal inflammation > increases likelihood of infection
25
Q

signs and symptoms of glue ear

A

most common = difficulty hearing and delay in speech and language development

in young children this may present with difficulty paying attention at school

other
- sensation of pressure in ear, popping or cracking noises
- recurrent acute otitis media
- less common = disequilibrium and vertigo

26
Q

investigations and findings for glue ear

A

normally clinical!

can do otoscopy - tympanic membrane will be a dull yellowish tinge, may see bubble or fluid level behind TM

and hearing test/middle ear function test - conductive hearing loss, reduced membrane compliance

27
Q

management for glue ear

A

active surveillance - normally resolves within 3m

28
Q

management for glue ear if it’s persisted for 3m

A
  1. nonsurgical = hearing aid insertion
  2. surgical = myringotomy and grommet insertion
29
Q

what are grommets? where are they positioned?

A

tiny ventilation tubes inserted into the middle ear, positioned in the tympanic membrane

30
Q

what is the function of grommets?

A

helps to drain fluid build-up out of the middle ear > improved hearing

31
Q

how are grommets inserted? how long do they stay in for? how do they come out again?

A

inserted under GA
remain in for approx 6m
gradually pushed out (but may need to be removed under GA)

32
Q

which children are grommets indicated in?

A

those with repeated ear infections/glue ear

33
Q

causes of deafness:
a) congenital
b) perinatal
c) after birth

A

a) - maternal rubella/cytomegalovirus
- genetic deafness
- associated syndromes e.g. Down’s syndrome

b) - prematurity
- hypoxia during/after birth

c) - jaundice
- meningitis/encephalitis
- otitis media/glue ear
- chemo

34
Q

how would deafness present in a newborn?

A

during the UK Newborn Hearing Screening Programme (NHSP) - tests hearing in all neonates

35
Q

how may deafness present if not identified when a child is a neonate?

A
  • parental concerns
  • behavioural changes associated
  • ignoring calls/sounds
  • frustration of bad behaviour
  • poor speech and lang development
  • poor school performance
36
Q

investigations for deafness (assuming it was not picked up in neonatal screening) in children
a) <3
b) >3

A

a) tested by looking for basic response to sound e.g. turning head

b) tested with headphones, tones and volumes (audiometry, results recorded on an audiogram)

37
Q

how does an audiometry work? what is recorded on an audiogram?

A
  • plays sounds
  • documents the volume at which the pt hears the sound
  • the louder the sound required, the worse the hearing
  • frequency (hZ) on x-axis, volume (dB) on y-axis
38
Q

what range of decibels (dB) will be found on audiometry if the patient has:
a) normal hearing
b) sensorineural hearing loss
c) conductive hearing loss

A

a) 0-20dB

b) both air and bone conduction readings will be >20dB

c) bone conduction reading will be normal (0-20dB) but air conduction reading will be >20dB

39
Q

when are hearing aids indicated for deafness?

A

for children who still retain some hearing

40
Q

what is infantile haemangioma? which children is it common in? what does it look like?

A

also known as the ‘strawberry mark’

common in preterm babies/babies in SCBU

present as raised/bumpy red lumps, appearing in the first 4-6w of life

41
Q

what is the most common type of birthmark?

A

strawberry mark/infantile haemangioma

42
Q

complications of a strawberry mark

A

blindness/airway compromise if located on the eyes or mouth

43
Q

how are strawberry marks managed?

A

normally go away on their own

44
Q

naevus flammeus
a) also known as
b) when does it present
c) how does it present
d) management

A

a) port-wine stain birthmark
b) presents immediately from birth
c) flat, wine-coloured discolouration of the skin
d) no management - it never goes away

45
Q

what is a naevus? which conditions are associated with lots of them?

A

a mole!

e.g. Turner’s

46
Q

mongolian blue spots
a) when do they present
b) how and where do they present
c) who are they more common in

A

a) from birth
b) look like bruises, blue discolouration common on the bum
c) more common in children with pigmented skin

47
Q

a) what are cafe au lait patches?
b) what may they be a symptom of if there are many of them?

A

a) a common birthmark characterised by coffee-coloured patches varying in colour and size. v common for children to have one or two

b) multiple cafe au lait patches = symptom of neurofibromatosis (genetic disorder)

48
Q

a) what are milia?
b) what causes them?
c) how are they managed?

A

a) yellowish spots on the nose and cheek of infants
b) subaceous plugs from sweat glands
c) self-limiting

49
Q

stepwise management of anaphylaxis in children (7)

A

MANAGE BEFORE INVESTIGATING!

  1. ABCDE for diagnosis
  2. call for help
  3. remove suspected factors e.g. discontinue drug
  4. IM adrenaline into anterolateral thigh
  5. establish and maintain airway, give100% high flow O2
  6. if no response, repeat IM adrenaline after 5 minutes and give IV fluid bolus (crystalloid)
  7. if still no response, resus team
50
Q

why is a 2nd dose of adrenaline sometimes required when treating anaphylaxis?

A

it has a very short half-life

51
Q

what dose of adrenaline should be given in anaphylaxis management in:
a) children >12y
b) children 6-12y
c) children 6m-6y
d) children <6m

A

a) 500 microgram
b) 300 microgram
c) 150 microgram
d) 100-150 microgram

52
Q

what confirmatory blood test can be taken to confirm anaphylaxis? when would it be taken?

A

serum mast-cell trypase test

  • take ASAP once emergency tx started
  • second sample within 1-2 hours (no later than 4 hours) from onset of sx
  • then third sample 24h later/at FU to show baseline comparison

PHASE 3A (11 decks)

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