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1
Q

management for minimal change disease

A

60mg/m2/day prednisolone
fluid restrict and low salt diet

non responsive after 4-6 weeks
- tacrolimus, ciclosporine

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2
Q

management of henloch schonlein purpura

A

Monitor:
Urineanalysis
BP
FBC, U&Es, creatinine

Most will resolve spontaneously after 4 weeks
joint pain managed with analgaesia eg. paracetamol, ibruprofen

sever abdo pain, scrotal involvement, severe oedema: prednisolone

nephrotic rane proteinurea: IV corticosteroids

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3
Q

Investigations and managament of suspected UTI

A

temp >38 and symptoms in all ages –> refer to paeds

symptoms in <3month –> urgent referral

urinalysis
+NIT +LEUK –> treat as UTI, send MSU for culture if <3y, not first uti, suspected pyelonephritis
+NIT -LEUK –> treat as UTI, send MSU for culture
-NIT +LEUK –> send MSU for culture, <3yrs start abx, >3yrs consider Abx if clinically indicated
-NIT -LEUK –> UTI unlikely

ABx:
simple UTI –> Trimethoprim or nitrofurantoin
upper UTI/ pyelonephritis –> Cefalexin, co-amoxiclav

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4
Q

Mx and counseling of coeliac

A

what is it:
condition where the body sparks an immune response to gluten causing damage to the gut
if gluten is eaten it can be very serious and will cause lots of pain, D+V and damage but more importantly increases risk of certain cancer

what now:
Gastro referral
investigations to confirm diagnosis
FBC- anaemia and deficiencies- replace
anti-TTG Abs, anti-enomesyial
duodenal biopsy- villous atrophy, crypt hyperplasia, lymphocyte infiltration

what this means in the future:
life long avoidance of gluten: wheat, barley and rye containing products
dietician referral
pneumococcal vaccination as hyposplenic
screen for other autoimmune conditions
annual reviews: height and weight, review Sx and adherence to diet

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5
Q

management of croup

A

single dose of dexamethosone
0.15mg/kg
A-E assessment: O2 if required

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6
Q

Webbed neck
Pectus excavatum
Short stature
Pulmonary stenosis
male or female

A

Noonans syndrome

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7
Q

Learning difficulties
Macrocephaly
Long face
Large ears
Macro-orchidism

A

fragile X

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8
Q

Micrognathia
Low-set ears
Rocker bottom feet
Overlapping of fingers

A

Edwards syndrome

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9
Q

Microcephalic, small eyes
Cleft lip/palate
Polydactyly
Scalp lesions

A

pataus syndrome

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10
Q

Micrognathia
Posterior displacement of the tongue (may result in upper airway obstruction)
Cleft palate

A

Pierre robinsons syndrome

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11
Q

Hypotonia
Hypogonadism
Obesity

A

Prader willi syndrome

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12
Q

Short stature
Learning difficulties
Friendly, extrovert personality
Transient neonatal hypercalcaemia
Supravalvular aortic stenosis

A

Williams syndrome

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13
Q

features of: Prader Willi syndrome

A

obesity
hypogonadism
hypotonia

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14
Q

features of: Noonan’s syndrome

A

pulmonary stenosis
pectus excavatum
wide spaced nipples
short stature

similar to turners but can be boys AND girls where as turners is just girls

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15
Q

features of: Edwards syndrome

A

Roker bottom feet
microganthia
lowset ears
overlapping of fingers

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16
Q

features of: Pataus syndrome

A

polydactyle
abnormal facies
clef lip and palate
small eyes
short gap between eyes

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17
Q

features of: Turners syndrome

A

short stature
shield chest, widely spaced nipples
webbed neck
bicuspid aortic valve (15%), coarctation of the aorta (5-10%)
primary amenorrhoea
cystic hygroma (often diagnosed prenatally)
high-arched palate
short fourth metacarpal
multiple pigmented naevi
lymphoedema in neonates (especially feet)
gonadotrophin levels will be elevated
hypothyroidism is much more common in Turner’s
horseshoe kidney: the most common renal abnormality in Turner’s syndrome

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18
Q

features of: Williams syndrome

A

short stature
LD
extroverted and friendly personality
transient neonatal hypercalcemia
supravalvular aortic stenosis

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19
Q

features of: Pierre Robinson

A
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20
Q

Features of: fragile X syndrome

A

LD
long face

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21
Q

definition of status epilepticus

A

prolonged seizure (>30 minutes) or recurrent seizures without return to baseline between seizures

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22
Q

causes of status epilepticus

A

Common:
febrile convulsions
epilepsy

rarer:
hyponatraemia
hypocalcaemia
CNS infection
hypoglycaemia
raised ICP
CVA
toxin poisoning
inborn error of metabolism

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23
Q

urgent investigations for status epilepticus

A

Investigations:
 Finger prick blood glucose
 FBC, sodium, calcium, magnesium, urea, creatinine, CRP
 Ammonia if neonate/ suspect inborn error of metabolism
 Consider toxicology screen (esp. teenagers)
 Blood pressure (exclude malignant hypertension)
 CT if focal signs/ new focal seizure, trauma, possible VP
shunt complication or space occupying lesion

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24
Q

Managament of status epilepticus

A

ABCD
A- secure airway, call anaethesist if not able to protect for intubation
B- give high flow oxygen HYPOXIA BIGGEST CONCERN
C- Insert cannulae, monitor BP
D- fingerprick glucose

  1. IV access –>IV lorazepam 0.1mg/kg (max 4mg)
    no IV access –> buccal midazolam 0.5mg/kg (max 10mg) OR rectal diazepam 0.5mg/kg
  2. continued to seize
    IV lorazepam 0.1mg/kg
    or paraldehyde PR 0.8mL/kg 50:50 mix (then consider IV/ IO access)
  3. CALL SENIOR HELP
  4. patient not normally on phenytoin –> give Phenytoin 20mg/kg by IV/IO over 20mins
    usually on phenytoin –> Levetiracetam 30mg/kg IV/IO(max 3g)
  5. CALL ON CALL ANAETHESIST AND PICU
  6. Rapid sequence induction of anaesthesia: intubate and ventilate
    Propofol 2-4mg/kg IV

Important issues
 Glucose: aim for 4-8 mmol/L
 Hyponatraemia (Na <135)
if Na <135 mmol/L and still
seizing OR Na <130 mmol/L give
bolus 3 mL/kg 2.7% sodium
chloride
 Aim for temp <37oC
 Meningitis
Ceftriaxone 80 mg/kg IV
 Encephalitis: add aciclovir +
macrolide
 Raised ICP on CT or clinical
signs – Neuroprotect guide

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25
Q

signs of mild hypoxic ischaemic encephalopathy

A

irritability
startle reponses
poor feeding
hyperventilation

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26
Q

signs of moderate HIE

A

altered tone
reduced movement
seizures

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27
Q

causes of seizure in newborn

A

encephilitis/ meingitis
moderate-severe HIE
hypoglycaemia
hyponatraemia (eg. CAH)
other electrolyte imbalances

breath holding attacks
reflex anoxic seizures

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28
Q

diagnostic finding on EEG for absence seizure

A

3 spike waves per second in all leads

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29
Q

describe benign rolandic epilepsy

A

partial seizures
-> twitching, numbness or tingling of the child’s face or tongue, and may interfere with speech and cause drooling
-> child usually aware during seizure
seizures may become generalised
usually occur early in the morning
young children (6-8yrs) and tend to grow out of it by teens without treatment

may affect sleep and performance in school

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30
Q

loss of consciousness differentials

A

reflex anoxic seizure (baby/ toddler after being frightened or eg. bump on head)
BRUE (baby)
chocking on feeds
breath holding attacks (toddler- commonly after temper tantrum)
epilepsy
narcolepsy
vasovagal syncope
heart conditions eg. WPW, HOCM
hypoglycaemia

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31
Q

inflamed demyelinating HYPERINTENSE lesions in the white matter with changes in vision and loss of power indicative and urinary incontinence indicative of..

A

Multiple sclerosis

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32
Q

differentials for space occuplying lesions with surrounding oedema

A

brain tumour eg. glioma, neuroblastoma
TB
brain abscess

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33
Q

findings associated with tuberous sclerosis

A

Ash leaf macule

CT/MRI
sub epyndemal calcifications and hypointense white matter lesions

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34
Q

adverse risks in sickle cell disease

A

sickle cell painful crisis- blocked vessels leading to painful ischaemia

acute chest syndrome (usually brought on by infection)

avascular necrosis

blood clots- MI, stroke, DVT, PE

dactylitis - painful swollen fingers

infection- increased risk of infection due to damage of the spleen eg. flu, meningitis, pneumonia (must have pneumococcal, flu and meningococcal vaccines)

splenic sequestration- splenomegaly and pain from pooling of trapped blood

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35
Q

what is sickle cell disease

A

autosomal-recessive single gene defect in the beta chain of haemoglobin, which results in production of sickle cell haemoglobin (HbS).

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36
Q

management of acute painful (vaso occlusive) crisis in SCD

A
  1. analgaesia eg. paracetamol/ibruprofen/ naproxen (caution with liver or kidney damage) Coedine not recommended in young children CI in <12y
  2. O2 if required
  3. correction of any blood gas disturbance
  4. fluids if intravascularly depleted
  5. blood exchange for life threatening
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37
Q

management of acute chest crisis in SCD

A
  1. secure airway
  2. give oxygen if required
  3. broad spectrum antibiotics if infection after sending blood cultures
  4. paracetamol for pain
  5. fluids if necessary
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38
Q

side effect of sodium valporate

A

increased appetite
weight gain
hair loss
liver failure

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39
Q

side effects of carbamazepine

A

PATCH
Potentiates ADH -> water retention
Aplastic anaemia/ agranulocytosis
Teratogenic, transient leukopenia
CNS effects- eg. dizziness, ataxia, headache, visual disturbances
Hepatic transaminases elevated

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40
Q

side effects of lamotrigine

A

Rash
behavioural changes
irritability

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41
Q

side effects of vigabatrin

A

behavioural changes
retinopathy
sleep disturbances
weight gain

42
Q

side effeects of levetiracetam

A

anorexia
abdominal pain
vomiting
diarrhoea
behavioural changes
thrombocytopenia

43
Q

features of sturge weber syndrome

A

portwine stain on face
neurological defects - leptomeningeal angioma, seizures
glaucoma

44
Q

skin lesions and associated condition:

ash leaf macule
cafe au lait spots
portwine stain

A

ash leaf macule - tuberous sclerosis

cafe au lait spots - neurofibromatosis, McCune albright
portwine stain - Sturge-Weber syndrome

45
Q

nocturnal eneuresis management

A
  1. <5 reassure that will probably grow out of it

look for possible causes:
- DM
- constipation
- UTI
- high fluid intake

  1. positive reinforcement eg. gold stars, go to toilet before bed
  2. eneuresis alarm
  3. referral to specialist
  4. desmopressin
46
Q

what would be expected in each domain in a 6 week old

A

gross motor - lifts head 45 degrees from prone

fine motor - holds rattle if given

visual - fix and follows 180C

speech and language - startles at loud noise

social- smiles

47
Q

what would be expected in each domain in a 3 month old

A

gross motor -Lying on abdomen, good head control

fine motor -Reaches for object
Holds rattle briefly if given to hand
Visually alert, particularly human faces
Fixes and follows to 180 degrees

speech and language -Quietens to parents voice
Turns towards sound
Squeals

social- Laughs
Enjoys friendly handling

48
Q

what would be expected in each domain in a 6 month old

A

gross motor - sits unsupported back curved, rolls from prone to supine

fine motor - passess object from hand to hand

visual - points at object

speech and language - understands bye bye, no
babbles
turns head at loud sounds

social- put things in mouth (stops at 1yr), shaked rattle

49
Q

what would be expected in each domain in a 9 month old

A

gross motor - sits with straight back, walks with support

fine motor - immature pincer grip

visual - object permanence

speech and language -

social- scared of strangers (6months- 2 yrs)
bites food

50
Q

what would be expected in each domain in a 12 month old

A

gross motor - walks unsupported

fine motor - mature pincer grip, tower of 2 bricks

visual

speech and language - understands nouns (‘wheres mummy’)
3 words
points to body part

social- waves bye bye, plays alone, drinks from beaker with lid

51
Q

what would be expected in each domain in a 18 month old

A

gross motor - runs and jumps. red flag for not walking

fine motor - tower of 4
visual

speech and language - 1-6 words

social- imitates everyday activities

52
Q

what would be expected in each domain in a 2 year old

A

gross motor - up and down stairs two feet per step
walk on tip toes
throws ball

fine motor- tower of 8, turns multiple pages of book at a time, draws vertical line (horizontal at 2.5yrs)

visual

speech and language - 2 words together, 50 word repertoire

social- plays but doesnt share

53
Q

what would be expected in each domain in a 3 year old

A

gross motor - hopping, walks upstairs one foot per step, downstairs two feet per step

fine motor - builds bridge with blocks, turns one page of book at a time, draws circle

visual
speech and language - understands prepositions, 3-4words joined together

social- interactive play with sharing, eats with fork and spoon, plays without parents

54
Q

what would be expected in each domain in a 4 year old

A

gross motor - walks up and down stairs as an adult

fine motor - draws square/ cross
visual

speech and language - understands 2 step commands, complex sentences

social- sympathy for others if hurt, has a best friend, bladder control, imaginative play, dressing and undressing

55
Q

what would be expected in each domain in a 5 year old

A

gross motor

fine motor - draws triangle , buttons
visual

speech and language - tells a story using past tense

social- handles knife, takes turns, sings/dances/ acts

56
Q

differentials for delay in gross motor

A

cerebral palsy
duchenne muscular dystrophy
prader willi?

57
Q

differentials for delay in fine motor/ visual

A

visual impairment
dyspraxia
cerebral palsy

58
Q

differentials for delay in speech and language

A

hearing problems
neglect
ASD
learning difficulties
cerebral palsy (multiple)

59
Q

differentials for delay in social domain

A

neglect
ASD

60
Q

differentials for global developmental delay

A

down syndrome
fragile X
cerebral palsy

61
Q

red flags in development

A

no smile at 10 weeks
hand preference before 12 months
cant sit unsupported at 12 months
cant walk at 18 months

62
Q

management of suspected cerebral palsy

A

MDT approach: paediatrician, neurologist nurse, PT, OT, SALT, dietician, psychology

Aiming to improve quality of life
management varies from pr to pt

PT to help with walking
may give some muscle relaxants eg. botulin toxin injections
stiffnes- baclofen, diazepam

pain management using pain ladder

SALT for speech and swallowing

OT- identify struggles in every day tasks and find was to optomise

anticholinergics for saliva control

optomise sleep hygiene, melatonin

opthmalologist

63
Q

risk factors for cerebral palsy

A

prenatal:
chorioamnionitis
maternal infection
congenital infection eg. rubella, toxo, CMV
hypoxic brain injury eg. difficult labour
traumatic brain injury
meningitis

64
Q

classifications of cerebral palsy

A

spastic CP (70%)- lesion in cerebral cortex causing damage to UMN, reduced GABA causing increased tone and permanent flexion of muscle groups

dyskinetic- lesion in the basal ganglia and substantia nigra. issues with initiating and preventing movement- chorea and dystonia

ataxic- damage to the cerebellum causing ataxia, discoordination

65
Q

paediatric vital signs ranges (HR and RR)

A

<1
HR: 110-160
RR: 30-40

1-2
HR: 100-150
RR: 25-35

2-5
HR: 90-140
RR: 25-30

5-12
HR: 80-120
RR: 20-25

> 12
HR: 60-100
RR: 15-20

66
Q

what is the definitive management of pyloric stenosis

A

Ramstedt pyloromyotomy

67
Q

signs of non accidental injury

A

inconsistent story with injuries/ history keeps changing

repeated attendance to A&E (not GP)

child looks frightened

late presentation

physical:
- bruises in unusual places
- different bruises at different stages of healing
- bruising in a non mobile child
- failure to thrive

68
Q

management of neonatal sepsis

A

urgent admission and treatment on suspicion

Investigations:
- urinanalysis
- blood cultures
- FBC, CRP, LFTs, U&Es
- VBG/ABG
-LP

Treatment
- IV benzylpenicillin and gentamycin
- oxygen
- IV fluids and electrolyte maintenance
- prevension of hypoglycaemia

69
Q

Signs of neonatal sepsis

A

signs of resp distress: grunting, nasal flaring, recessions, tachpnoea (85%)
apnoea (40%)
change in mental state, lethargy
jaundice (35%)
reduced feeding (30%)
vomiting (25%)
abdo distension (20%)

70
Q

murmur is described as a ‘continuous blowing noise’ heard below both clavicles.

A

venous hum

71
Q

causes of snoring in children

A

obesity
downs syndrome
tonsilitis
nasal problems: polyps, deviated septum, hypertrophic nasal turbinates
hypothyroidism

72
Q

dose of dex in croup

A

0.15mg/kg

73
Q

features of congenital rubella

A

sensorineural deafness
cataracts
CHD (PDA)
glaucoma

Growth retardation
Hepatosplenomegaly
Purpuric skin lesions
‘Salt and pepper’ chorioretinitis
Microphthalmia
Cerebral palsy

74
Q

features of congenital toxoplasmosis

A

cerebral calcification
corioretinitis
anaemia
hepatosplenomegaly
hydrocephalus
cerebral palsy

75
Q

features of congenital CMV

A

microcephaly
Low birth weight
sensorineural deafness
purpuric rash
visual impairments
anaemia
hepatosplenomegaly
jaundice
encephalitis
pneumonitis
learning disabilities
cerebral palsy

76
Q

what is in the 6-in-1 vaccine and when is it given?

A

who did the path haematology help?

whopping (pertussis)
diptheria
tetanus
polio
haemophilius influenzae
hepatitis B

2,3 and 4 months

77
Q

whats in the 4-in-1 and whens it given?

A

who did the path

whopping
diptheria
tetanus
polio

3-4years

78
Q

whats in the 3-in-1 and whens it given?

A

did the path

diptheria
tetanus
polion

13-18years

79
Q

when is MMR given

A

12 months and booster at 3-4years

80
Q

when is MenB given?

A

2,4 and 12 months

81
Q

whens the pneumococcal vaccine given?

A

3 months and 12 months

82
Q

when is menACWY given?

A

pre uni/ 13-18yrs

83
Q

when is HPV given?

A

12-13 years to girls and boys

84
Q

what is the difference between Men ABCWY?

A

N meningitidis is classified into different serogroups based on the components that make up the polysaccharide capsule. The different vaccines therefore encompass different surface antigens specific for the different serogroups

there are 6 main serogroups that casue invasive meningococcal disease

85
Q

What are tet spells and what can be a quick method to improve

A

increase in O2 demand leading to cyanosis. usually happens during feeding or crying

bending of legs kinks the femoral arteries and increases vascular resistance which increases BP and increases the pressure in the left side, reversing the VSD shunt

86
Q

murmur heard in tetralogy of fallot

A

pulmonary outflow obstruction
–> ejection systolic murmur heard loudest at left sternal edge

87
Q
  1. what is the most common complication of measles?
  2. what is the most common cause of death as a complication of measles?
A
  1. otitis media
  2. pneumonia
88
Q

cyanotic congenital heart defects

A

5Ts+H

Transposition of the great arteries
Tricuspid atresia
Tetralogy of fallot
Trunctus arteriosus
Total anomalous pulmonary venous connection (TAPVC)

+ hypoplastic left heart syndrome

89
Q

Features of Transposition of the great arteries

A

cyanosis noticed almost immediately
no improvement with saturations
loud S2
egg on a string appearance on CXR

associated with maternal diabetes

90
Q

management of TGA

A
  1. maintenance of PDA with prostaglandin E2
    - NICU/PICU
  2. surgical fixation
91
Q

features of tricuspid atresia

A

valve doesnt form so no blood flow in RV so it doesnt develop (hypoplastic)
VSA/ ASD and PDA
cyanotic baby noticed in days of birth
ejection systolic murmur

92
Q

features of TOF

A
  1. Pulmonary outflow tract obstruction (eg. stenosis)
  2. hypertrophy of right ventricle
  3. VSD
  4. overriding aorta

cyanosis noticed in weeks/ months
boot shaped heart on CXR
harsh sings systolic ejection murumur ans single S2

93
Q

murmur heard in ebsteins anomaly

A

pansystolic (tricuspid regurg) and mid diastolic (tricuspid stenosis)

94
Q

features of fetal alcohol syndrome

A

microcephaly (small head)
short palpebral fissures (small eye opening)
hypoplastic upper lip (thin)
absent philtrum
reduced IQ
variable cardiac abnormalities.

95
Q

what are some signs of DMD?

A

delayed walking
calf pseudohypertrophy
Gowers sign (using hands to help stand)
30% have LD

later
wheelchair
respiratory distress from weak diaphragm
dilated cardiomyopathy

96
Q

difference between duchenne and becker muscular dystrophy

A

same dystrophin gene but duchenne is when there is absence of dystrophin and beckers is mishapen dystrophin

duchenne- presents by 5yrs
beckers- presents by 10-20

97
Q

what is the prognosis of DMD?

A

most will be fully wheelchair bound by 12

life expectancy of around 25-30

98
Q

criteria for immediate CT after head injury

A

Loss of consciousness lasting more than 5 minutes (witnessed)

Amnesia (antegrade or retrograde) lasting more than 5 minutes

Abnormal drowsiness

Three or more discrete episodes of vomiting

Clinical suspicion of non-accidental injury

Post-traumatic seizure but no history of epilepsy

GCS less than 14, or for a baby under 1 year GCS (paediatric) less than 15, on assessment in the emergency department

Suspicion of open or depressed skull injury or tense fontanelle

Any sign of basal skull fracture (haemotympanum, panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)

Focal neurological deficit
If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head

Dangerous mechanism of injury (high-speed road traffic accident either as pedestrian, cyclist or vehicle occupant, fall from a height of greater than 3 m, high-speed injury from a projectile or an object)

99
Q

list the features of meckels diverticulum
(rule of 2)

A

2% of population
2% symptomatic
2x more common in males
2 years old
2 feet from iliocaecal valve
2 inches long
2/3rds have ectopic tissue
2 types of ectopic - gastric and pancreatic mucosa

100
Q

symptoms of meckels diverticulum

A

abdominal pain mimicking appendicitis
rectal bleeding
Meckel’s diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
intestinal obstruction
secondary to an omphalomesenteric band (most commonly), volvulus and intussusception

101
Q

investigations and management of meckels

A

abdo USS
technitium pertechnetate 99 scan
mesenteric angiography

Mx
may require transfusion if haemodynamically unstable
Surgery- wedge excision or bowel resection and anastamosis

Paeds (3 decks)

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