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FINALS REVISION > Paeds > Flashcards

Paeds Flashcards

1
Q

what is croup

A

viral laryngotracheobronchitis

stridor caused by laryngeal oedema and secretions

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2
Q

which organisms cause croup

A

parainfluenza viruses

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3
Q

when is croup more common

A

autumn

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4
Q

what are the symptoms/signs of croup

A

stridor
barking cough
fever
coryzal symptoms

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5
Q

how is croup diagnosed

A

clinically

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6
Q

what might you see on cxr of croup

A

PA view shows subglottic narrowing (steeple sign)

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7
Q

what treatment for croup

A

oral dex 0.15mg/kg

admit if stridor at rest

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8
Q

what emergency treatment for croup

A

high flow o2

nebulised adrenaline

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9
Q

what causes epiglottitis

A

haemophilus influenzae type b

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10
Q

what are symptoms of epiglottitis

A

fever
stridor
drooling
tripod position

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11
Q

how is epiglottitis diagnosed

A
  • clinical by trained airway staff
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12
Q

what sign on epiglottitis xray

A

lateral view - thumb sign - swelling of epiglottis

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13
Q

what management of epiglottitis

A

immediate senior involvement
endotracheal intubation may be necessary to secure airway
oxygen
cefotaxime IV

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14
Q

what type of vasculitis is kawasaki

A

medium vessel

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15
Q

what are symptoms of kawasaki

A
  • fever resistant to antipyretics
  • cervical lymphadenopathy
  • conjunctival injection
  • bright red cracked lips
  • strawberry tongue
  • palmar, sole erythema, desquamation
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16
Q

how is kawasaki managed

A

high-dose aspirin
IVIg
echocardiogram to screen for coronary artery aneurysm

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17
Q

How is duchenne’s transmitted, what gene?

A

x linked recessive inherited disorder of dystrophin genes on xp21

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18
Q

what are the symptoms of duchennes

A
  • proximal muscle weakness
  • calf pseudohypertrophy
  • Gower’s sign
  • some patients have intellectual impairment
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19
Q

what investigations for muscular dystrophies

A 
genetic testing (replaced muscle biopsy)
creatinine kinase
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20
Q

what management for muscular dystrophies

A

supportive

oral steroids can delay progression weakness
creatinine supplements can give some improvement in muscle strength

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21
Q

what condition associated with duchenne’s

A

associated with dilated cardiomyopathy

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22
Q

how is beckers muscular dystrophy inherited

A

x linked recessive, although dystrophin gene not as severely affected as in duchennes

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23
Q

how is beckers different to duchennes and how are they managed

A

symptoms appear later (8+ y) in becker than duchenne

mgmt similar to duchennes

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24
Q

what is immune thrombocytopaenic purpura

A

immune mediated reduction in platelet count

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25
Q

what are antibodies directed against in ITP and what type of hypersensitivity reaction is this

A

GP IIb/IIIa or Ib-V-IX complex

type 2 hypersensitivity

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26
Q

how does ITP present

A

usually following viral illness or vaccination

bruising
purpuric rash
bleeding less common (gingival/epistaxis)

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27
Q

how is ITP investigated

A

FBC - isolated thrombocytopaenia
blood film
bone marrow studies only if atypical features such as lymphadenopathy, splenomegaly or if failure to resolve

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28
Q

when would bone marrow studies be indicated in ITP and what would they show

A

lymph node enlargement
splenomegaly
failure to respond to treatment/resolve

megakaryocytes

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29
Q

what mgmt of ITP

A

usually resolves by 6mths

oral/IV steroids
IVIg
platelet transfusion if active haemorrhage

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30
Q

explain pathophys of hirschsprung’s

A

aganglionic segment of bowel due to developmental failure of parasympathetic auerbach’s and meissner plexuses

uncoordinated peristalsis -> obstruction

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31
Q

what is hirschsprung’s associated with

A

down’s

more common in males

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32
Q

how would hirschsprungs present

A

failure to pass meconium by 3 days

constipation, abdo distension

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33
Q

how is hirschsprungs diagnosed

A

AXR

gold standard: rectal biopsy

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34
Q

how is hirschsprung’s managed in the immediate setting and definitively

A

immediate: rectal irrigation to prevent enterocolitis

definitive - surgical resection of affected segment of bowel

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35
Q

what is congenital diaphragmatic hernia

A

incomplete formation of diaphragm

herniation of abdominal viscera into thoracic cavity causing pulmonary hypoplasia and hypertension

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36
Q

how would congenital diaphragmatic hernia present

A

respiratory distress
tinkling bowel sounds in thorax
absent heart sounds on left hand side

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37
Q

what is best initial mgmt of congenital diaphragmatic hernia

A

intubate and ventilate

NG tube to prevent air going into the stomach

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38
Q

what is gastroschisis?

A

congenital defect in anterior abdominal wall just lateral to the umbilicus

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39
Q

what is the management of gastroschisis

A

vaginal delivery

immediate surgical correction (within 4 hours)

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40
Q

what is exomphalos

A

abdo contents protrude through abdo wall but are covered in amniotic sac covered in amniotic membrane and peritoneum

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41
Q

how is exomphalos managed

A

c-section to decrease chance of rupture

staged surgical correction

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42
Q

what is exomphalos associated with

A

down’s
beckwith wiedemann syndrome
cardiac and renal problems

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43
Q

what is gastroschisis associated with

A

socioeconomic deprivation - smoking, drinking during preg

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44
Q

how is candidal nappy rash treated

A

topical imidazole

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45
Q

how do infantile spasms present

A

flexion of head arms trunk followed by extension of arms

progressive mental handicap

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46
Q

what investigations for infantile spasms

A

EEG - hypsarrhythmia

CT - diffuse/localised brain disease eg. tuberous sclerosis

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47
Q

how is infantile spasms treated

A

vigabatrin

ACTH/pred

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48
Q

what is necrotising enterocolitis

A

disorder affecting prem neonates where a segment of bowel becomes necrotic

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49
Q

what RFs for nec

A 
very low birth weight
formula feed
respiratory distress/assisted ventilation
sepsis
PDA and congenital heart disease
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50
Q

how would NEC present

A 
bilious vomiting
intolerance to feeds
distended tender abdomen
blood in stools
absent bowel sounds
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51
Q

how would perforated NEC present

A

peritonitis and shock, severely unwell neonate

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52
Q

what investigations for NEC

A

AXR

bloods - FBC, CBG, blood cultures, CRP

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53
Q

what would AXR show in NEC

A
  • dilated loops of bowel
  • gas in the bowel wall (pneumatosis intestinalis)
  • bowel wall oedema
  • gas in the peritoneal cavity if perforated (pneumoperitoneum)
  • gas in portal veins
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54
Q

how is NEC managed

A
  • NBM, IV fluids, total parenteral nutrition
  • antibiotics
  • immediate referral to neonatal surgical team for:
  • surgical removal of necrotic bowel
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55
Q

what would CBG of NEC show

A

metabolic acidosis

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56
Q

what is pityriasis versicolour (aka tinea versicolour)

A

superficial cutaneous fungal infection caused by malassezia furfur

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57
Q

how does pityriasis versicolour present

A

affects trunks
hypopigmented/pink/brown lesions
scaly
mild pruritus

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58
Q

what are RFs for pityriasis versicolour

A
  • immunosuppression
  • cushing’s disease
  • malnutrition
59
Q

what treatment for pityriasis versicolour

A

topical ketoconazole

if persistent - oral itraconazole

60
Q

what is pityriasis rosea

A

acute self-limiting rash affecting young adults

thought to be linked to HHV-7 (herpes hominis)

61
Q

how does pityriasis rosea present

A
  • some prodromal viral illness
  • herald patch on trunk
  • followed by erythematous oval scaly patch in fir tree distribution
62
Q

how is pityriasis rosea treated

A

self-limiting within 6-12 weeks

63
Q

what are RFs for developing epilepsy following febrile convulsions

A
  • family history of epilepsy
  • complex febrile seizures
  • background of neurodevelopmental disorder
64
Q

what is biliary atresia

A

atresia/occlusion of biliary ducts

65
Q

how does biliary atresia present

A
  • obstructive jaundice after 2 weeks
  • dark urine and pale stool
  • appetite and growth disturbance
66
Q

what signs would you find on examination of biliary atresia

A
  • hepatosplenomegaly
  • jaundice
  • abnormal growth
  • cardiac murmurs (associated with cardiac abnormalities)
67
Q

what investigations for biliary atresia

A
  • serum bilirubin - total bilirubin may be normal, but conjugated is VERY HIGH
  • LFTs cannot differentiate between causes of jaundice
68
Q

what management of biliary atresia

A

surgical - kasai portoenterostomy

or liver transplant

69
Q

what complications of biliary atresia

A

cirrhosis
portal hypertension
liver failure

70
Q

why does biliary atresia not cause kernicterus

A

liver is still able to conjugate bilirubin. conjugated bilirubin is unable to cross BBB

71
Q

what vitamin deficiencies are associated with biliary atresia and how would this present

A

ADEK, fat soluble vitamins
failure to thrive
bleeding

72
Q

what is osteomalacia

A

softening of bones secondary to vit D deficiency

73
Q

which organism causes measles

A

RNA paramyxovirus

74
Q

what are the symptoms of measles

A

prodromal:

  • fever
  • irritability
  • conjunctivitis
  • koplik spots
  • rash - macpap starts behind ears and spreads, becomes confluent
  • some desquamation sparing palms and soles

10% get diarrhoea

75
Q

what are the complications of measles

A 
otitis media
pneumonia
encephalitis
subacute sclerosing panencephalitis
corneal ulceration/keratoconjunctivitis
diarrhoea
increased incidence of appendicitis
myocarditis
76
Q

what investigation for measles

A

IgM antibodies

77
Q

what mgmt for measles

A

supportive

if preg/immunosuppressed admit

78
Q

what mgmt for measles contacts

A

MMR vax within 72 hours (vax immunity develops faster than natural immunity)

79
Q

what causes mumps

A

RNA paramyxovirus

80
Q

what symptoms of mumps

A
  • fever
  • malaise/muscle aches
  • parotitis - ear pain, pain on eating. unilateral -> bilateral
81
Q

what complications of mumps

A
  • orchitis
  • hearing loss (unilateral, transient)
  • meningoencephalitis
  • panencephalitis
  • pancreatitis
82
Q

what treatment for mumps

A

supportive, PHE notification

83
Q

when is mumps infectious

A

7 days before parotitis and 9 days after

84
Q

how is mumps spread

A

droplets

respiratory tract epithelial cells -> parotid cells -> other tissues

85
Q

what topical Abx if resistance suspected for impetigo

A

mupirocin

oral fluclox/erythromycin if systemic infection

86
Q

what is bullous impetigo

A
  • caused by staph aureus bacteria releasing epidermolytic toxins causing vesicles to form

vesicles burst and release exudate forming golden crust without scarring

87
Q

what is staphylococcus scalded skin syndrome

A

extensive bullous impetigo

88
Q

what treatment for bullous impetigo/staph scalded skin syndrome

A

oral/IV fluclox

89
Q

what complications of impetigo if caused by strep pyogenes

A

post-streptococcal glomerulonephritis

scarlet fever

90
Q

what causes rubella

A

togavirus

91
Q

what are the symptoms of rubella

A

fever
macpap rash starts on face and spreads
lymphadenopathy - suboccipital and post-auricular

92
Q

what are the complications of rubella

A

arthritis
thrombocytopaenia
encephalitis
myocarditis

93
Q

what are the features of congenital rubella syndrome

A
  • sensorineural deafness
  • congenital heart disease eg PDA
  • congenital cataracts
  • salt and pepper chorioretinopathy
  • micropthalmia
  • purpuric skin lesions
  • cerebral palsy
  • growth retardation
  • hepatosplenomegaly
94
Q

how should cases of rubella in preg be managed

A

discuss with local health protection unit
avoid contact with other pregnant women
offer MMR vaccine post-natally

95
Q

what causes chickenpox

A

varicella zoster virus

96
Q

how is chickenpox spread

A

respiratory

97
Q

how does chickenpox present

A

fever
itchy rash - mac then pap then vesicular
mild systemic upset (fatigue, malaise)

98
Q

how is chickenpox managed

A

trim nails, keep cool

calamine lotion/chlorphenamine for itching

99
Q

how is chickenpox isolated?

A

until all lesions have dried and crusted over, usually about 5 days from onset of rash

100
Q

what are the complications of chickenpox

A
  • secondary bacterial infection
  • group A strep -> necrotising fasciitis
  • pneumonia
  • encephalitis - ataxia
  • disseminated haemorrhagic chickenpox
  • pancreatitis
  • arthritis
  • nephritis
  • conjunctival lesions
101
Q

how does chickenpox encephalitis present

A

ataxia

102
Q

where does chickenpox virus lie dormant

A

sensory dorsal root ganglion and cranial nerves

103
Q

how do you manage chickenpox exposure in preg

A

check blood urgently for varicella antibodies
if none
<20 weeks - VZIG immediately
>20 weeks - aciclovir 10-14 days post exposure

104
Q

how do you manage confirmed chickenpox in preg

A

seek specialist advice

if rash - acyclovir. use with caution in <20 weeks

105
Q

how does fetal varicella syndrome present

A 
skin scarring
microcephaly
micropthalmia
limb hypoplasia
learning difficulties
106
Q

what are the complications of maternal chickenpox exposure

A

fetal varicella syndrome
severe neonatal varicella
neonatal shingles

107
Q

who is vaccinated against whooping cough and when

A

children and pregnant women 16-32 weeks

108
Q

how does whooping cough present

A 
fever
cough lasting 14+ days
cough, worse at night, paroxysmal cough
inspiratory whoop
post-tussive vomiting
apnoeic attacks in young infants
109
Q

how is pertussis diagnosed

A

nasal swab with PCR/bacterial culture

110
Q

how is pertussis managed

A
  • if under 6m, admit
  • notifiable disease
  • macrolide if <21 days (clarithromycin, erythromycin in preg)
111
Q

which antibiotics for pertussis in normal/preg

A

clarithromycin
erythromycin if preg

co-trimoxazole

112
Q

what are the complications of whooping cough

A
  • bronchiectasis
  • subconjunctival haemorrhages
  • pneumonia
  • seizures
  • pneumothorax
113
Q

how should household contacts of pertussis be managed

A 
prophylactic antibiotics (clari/erythromycin)
offer pertussis vaccine
114
Q

how long exclusion for whooping cough

A

21 days from onset of cough

48 hours after starting Abx

115
Q

what are the causes of cerebral palsy

A

antenatal:

  • maternal infections
  • trauma in pregnancy

perinatal

  • birth asphyxiation
  • pre-term birth

postnatal:

  • meningitis
  • head injury
  • severe neonatal jaundice
116
Q

what are the different types of cerebral palsy

A

spastic (UMN damage)
dyskinetic (basal ganglia damage)
ataxic (cerebellar damage)
mixed

117
Q

what symptoms of spastic cerebral palsy

A

spasticity, UMN signs - hyperreflexia, hypertonia, power same or reduced

118
Q

what symptoms of dyskinetic cerebral palsy?

A

athetoid movements
problems controlling muscle tone (hyper and hypotonia)
oro-motor problems

119
Q

what symptoms of ataxic cerebral palsy?

A

problems with coordinated movement and cerebellar signs

120
Q

what is extrapyramidal cerebral palsy?

A

another word for dyskinetic cerebral palsy

so is athetoid cerebral palsy

121
Q

how is cerebral palsy managed

A

multi-disciplinary team approach

  • baclofen PO/ intrathecal for spasticity
  • botox for spasticity
  • selective dorsal rhizotomy for spasticity
  • tenotomy for contractures
  • glycopyrrhonium for secretions
  • antiepileptics for seizures
122
Q

what treatment for hypoxic-ischaemic encephalopathy (HIE)

A

therapeutic cooling to target of 33-34, rectal temp probe

follow up by paediatrician and MDT

123
Q

what can cause HIE?

A
  • maternal shock
  • intrapartum haemorrhage
  • cord prolapse
  • nuchal cord
124
Q

what are the symptoms/signs of HIE?

A

mild:

  • irritabilty
  • hyper-alert
  • poor feeding

moderate:

  • poor feeding
  • hypotonic
  • seizures
  • lethargic

severe:

  • flaccid, reduced/absent reflexes
  • reduced consciousness
  • apnoeas
125
Q

what management of GORD in infancy

A

advise re: positioning, burping after feeds, sleep on back
trial of feed thickeners
alginates, but not alongside thickeners
PPI

126
Q

what causes of neonatal jaundice in first 24 hours

A
  • rhesus haemolytic disease
  • ABO haemolytic disease
  • hereditary spherocytosis
  • G6PD deficiency
  • sepsis
  • TORCH
    Toxoplasmosis
    CMV
    Rubella
    Syphillis
    Hepatitis
    Herpes
127
Q

what causes of neonatal jaundice 24h-14 days

A

physiological, haemolysis of fetal RBC
breast milk jaundice
breastfeeding jaundice
infection

128
Q

what causes of neonatal jaundice after 14 days

A

unconjugated - hypothyroidism, infection - UTI

conjugated - biliary atresia/neonatal hepatitis

129
Q

what causes kernicterus

A

high levels of unconjugated bilirubin cross BBB, depositing in the deep grey matter of brain and in basal ganglia causing encephalopathy

130
Q

what are some possible features of chronic kernicterus

A 
cerebral palsy
sensorineural hearing loss
gaze palsy
learning difficulties
death
131
Q

how would acute kernicterus present

A 
lethargy
irritability
abnormal muscle tone/posture
convulsions
apnoeic episodes
132
Q

what is physiological jaundice

A

fetal RBC have shorter lifespan than adult FBC (70 days vs 120)
increased RBC breakdown increases circulating bilirubin
hepatic bilirubin metabolism is less efficient in first few days of life
jaundice

133
Q

what is breast milk jaundice

A

not fully understood, thought to be due to levels of beta-glucoronidase in breast milk, blocking UGT, decreased metabolism of bilirubin causing jaundice

134
Q

what is breastfeeding jaundice

A

poor feeding, presents alongside dehydration

poor feeding causes reduced bilirubin excretion, increases enterohepatic circulation, more bilirubin enters system

135
Q

what is crigler-najjar

A

Congenital unconjugated hyperbilirubinaemia
no UGT enzyme activity
no conjugation of bilirubin
causes kernicterus and d

136
Q

what is gilbert syndrome

A

autosomal recessive condition causing defective conjugation of bilirubin

unconjugated hyperbilirubinaemia (not in urine)

presents with jaundice in fasting/illness/exercise

no treatment necessary

137
Q

what is g6pd deficiency

A

x-linked recessive g6pd deficiency

causing increased oxidative stress and intravascular haemolysis

138
Q

what triggers in g6pd

A

fava beans
sulfa drugs, ciprofloxacin
anti-malarials
infections

139
Q

what is associated with g6pd

A

splenomegaly

gallstones

140
Q

what investigations for g6pd

A

blood film - heinz bodies, bite and blister cells

g6pd enzyme assay

141
Q

what investigations for neonatal jaundice

A

FBC and blood film
conjugated bilirubin
blood type testing of mother and baby for ABO/Rh incompatibility
direct coomb’s test (direct antiglobulin for haemolysis)
TFT
blood cultures and urine dip
G6PD enzyme assay

142
Q

which brain haemorrhage is most common in prem infants and not associated with NAI

A

intraventricular haemorrhage

143
Q

what mgmt for neonatal jaundice

A

dxfjkhs

144
Q

what is tof

A 
PROV 
Pulmonary stenosis
Right ventricular hypertrophy
Overriding aorta
Ventricular septal defect

FINALS REVISION (17 decks)

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