Paediatric Common Conditions 1 Flashcards

1
Q

What is achondroplasia?

A

Achondroplasia is an autosomal dominant disorder associated with short stature

mutation in the fibroblast growth factor receptor 3 (FGFR-3) gene

This results in abnormal cartilage giving rise to:
short limbs (rhizomelia) with shortened fingers (brachydactyly)
large head with frontal bossing and narrow foramen magnum
midface hypoplasia with a flattened nasal bridge
‘trident’ hands
lumbar lordosis

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2
Q

What is acute epiglottitis? Presentation?

A

rare but serious infection caused by Haemophilus influenzae type B

Causes inflammation of the epiglottis

Features:
rapid onset
high temperature, generally unwell
stridor
drooling of saliva
‘tripod’ position

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3
Q

How can acute epiglottitis be diagnosed?

A

direct visualisation (only by senior/airway trained staff)

x-rays may be done, particularly if there is concern about a foreign body:
a lateral view in acute epiglottis will show swelling of the epiglottis - the ‘thumb sign’
PA view in croup will show subglottic narrowing, commonly called the ‘steeple sign’

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4
Q

How can acute epiglottitis be managed?

A

immediate senior involvement, including those able to provide emergency airway support (e.g. anaesthetics, ENT)

endotracheal intubation may be necessary to protect the airway

if suspected do NOT examine the throat due to the risk of acute airway obstruction

(the diagnosis is made by direct visualisation but this should only be done by senior staff who are able to intubate if necessary)

oxygen, IV antibiotics (ceftriaxone) , dexamethasone

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5
Q

What is the main complication to be aware of with epiglottitis?

A

epiglottic abscess, which is a collection of pus around the epiglottis

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6
Q

What is the most common malignancy affecting children?

A

Acute lymphoblastic leukaemia ( ALL)

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7
Q

How does ALL present?

A

anaemia: lethargy and pallor
neutropaenia: frequent or severe infections
thrombocytopenia: easy bruising, petechiae

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8
Q

Poor prognostic factors in ALL?

A

age < 2 years or > 10 years
WBC > 20 * 109/l at diagnosis
T or B cell surface markers
non-Caucasian
male sex

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9
Q

What are the key differentials for acute scrotal pain in children?

A

Testicular torsion - Most common around puberty
Irreducible inguinal hernia - Most common in children < 2 years old
Epididymitis - Rare in prepubescent children

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10
Q

Alpha-thalassaemia is due to a deficiency of alpha chains in haemoglobin.

Clinical severity depends on the number of alpha globulin alleles affected:

A

1/ 2 alpha globulin alleles affected = hypochromic and microcytic, Hb level is typically normal

3 alpha globulin alleles affected = hypochromic microcytic anaemia with splenomegaly, Hb H disease

If all 4 alpha globulin alleles are affected (i.e. homozygote) = death in utero (hydrops fetalis)

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11
Q

The Apgar score is used to assess the health of a newborn baby. At what times should it be used?

A

at 1, and 5 minutes of age

If the score is low then it is again repeated at 10 minutes

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12
Q

What are the APGAR criteria?
What are the normal values?

A

Activity (muscle tone)
Pulse
Grimace (reflex irritability)
Appearance (skin colour)
Respiratory effort

score of 0-3 is very low, between 4-6 is moderate low and between 7 - 10 means the baby is in a good state

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13
Q

How would you score activity (muscle tone) in the APGAR assessment?

A

active movement = 2
limb flexion = 1
flaccid = 0

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14
Q

How would you score pulse in the APGAR assessment?

A

> 100 = 2
< 100 = 1
absent = 0

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15
Q

How would you score grimace (reflex irritability) in the APGAR assessment?

A

Cries on stimulation/sneezes, coughs = 2
Grimace = 1
Nil = 0

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16
Q

How would you score appearance (skin colour) in the APGAR assessment?

A

pink = 2
body pink, extremities blue = 1
blue all over = 0

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17
Q

How would you score respiratory effort in the APGAR assessment?

A

strong, crying = 2
weak, irregular = 1
nil = 0

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18
Q

Which children with appendicitis are more likely to present atypically?

A

Children who are younger or have a retrocaecal/pelvic appendix

Appendicitis is uncommon in children under 4 years old but in this group often presents with perforation

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19
Q

What is classified as a severe asthma attack in children?

A

SpO2 < 92%

PEF 33-50% best or predicted

Too breathless to talk or feed

Heart rate
>125 (>5 years)
>140 (1-5 years)

Respiratory rate
>30 breaths/min (>5 years)
>40 (1-5 years)

Use of accessory neck muscles

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20
Q

What is classified as a life threatening asthma attack in children?

A

SpO2 <92%

PEF <33% best or predicted

Silent chest

Poor respiratory effort

Agitation

Altered consciousness

Cyanosis

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21
Q

Children with severe or life threatening asthma should be transferred immediately to hospital. Which children should you measure PEF in?

A

Children over 5

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22
Q

How should children with mild to moderate acute asthma be managed?

A

Bronchodilator therapy:
give a beta-2 agonist via a spacer (for a child < 3 years use a close-fitting mask)
give 1 puff every 30-60 seconds up to a maximum of 10 puffs
if symptoms are not controlled repeat and refer to hospital

Steroid therapy:
should be given to all children with an asthma exacerbation
treatment should be given for 3-5 days

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23
Q

What dose of prednisolone is given in kids with acute asthma?

A

1-2 mg/kg od (max 40mg)

OR

2 - 5 years = 20 mg od
> 5 years = 30 - 40 mg od

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24
Q

How should newly diagnosed asthma v newly diagnosed asthma with symptoms >= 3 / week or night-time waking be managed?

A

Newly diagnosed asthma = SABA

More symptomatic = SABA + paediatric low-dose inhaled corticosteroid (ICS)

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25
Q

What is the stepladder of mx for asthma in kids?

A

SABA

SABA + paediatric low-dose inhaled corticosteroid (ICS)

SABA + paediatric low-dose ICS + LTRA (e.g. montelukast)
SABA + paediatric low-dose ICS + LABA (e.g. Serevent- salmeterol)

In contrast to the adult guidance, NICE recommend stopping the LTRA at this point if it hasn’t helped

SABA + switch ICS/LABA for a maintenance and reliever therapy (MART)

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26
Q

What is Maintenance and reliever therapy (MART) ?

A

a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required

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27
Q

What is considered as a low dose ICS in kids?

A

<= 200 micrograms budesonide or equivalent

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28
Q

What is the stepladder for asthma mx in children under 5 years?

A

SABA

SABA + an 8-week trial of paediatric MODERATE-dose ICS

After 8-weeks stop the ICS and monitor the child’s symptoms:
if symptoms reoccur within 4 weeks of stopping ICS treatment, restart the ICS at a paediatric low dose as first-line maintenance therapy
if symptoms reoccur beyond 4 weeks after stopping ICS treatment, repeat the 8‑week trial of a paediatric moderate dose of ICS

SABA + paediatric low-dose ICS + LTRA

Referral for specialist assessment

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29
Q

What is ADHD?

A

Attention deficit hyperactivity disorder

a condition incorporating features relating to inattention and/or hyperactivity/impulsivity that are persistent

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30
Q

Give some features that might suggest “hyperactivity” ( ADHD criteria)

A

Unable to play quietly
Talks excessively
Does not wait their turn easily
Will spontaneously leave their seat when expected to sit
Is often ‘on the go’
Often interruptive or intrusive to others
Will answer prematurely, before a question has been finished
Will run and climb in situations where it is not appropriate

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31
Q

How can ADHD be managed?

A

ten-week ‘watch and wait’ period following presentation

Secondary care referral if sxs continue

Drug therapy should as a last resort and is only available to those aged 5 years +
Methylphenidate is first line and should initially be given on a 6 week trial basis
Dexamfetamine and Atomoxetine are also available

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32
Q

What is Methylphenidate’s mechanism of action? ADRs? How should patients be monitored?

A

CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor

ADRs: abdominal pain, nausea and dyspepsia

In children, weight and height should be monitored every 6 months
ECG before starting as cardiotoxic

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33
Q

What is autism?

A

a neurodevelopmental condition characterized by qualitative impairment in social interaction and communication as well as repetitive stereotyped behaviour, interests, and activities.

three to four times more common in boys than girls

typically evident before 2–3 years of age

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34
Q

What clinical features may autism present with?

A

Impaired social communication and interaction:
- Children frequently play alone and maybe relatively uninterested in being with other children
- may fail to regulate social interaction with nonverbal cues like eye gaze, facial expression, and gestures
- Fail to form and maintain appropriate relationships and become socially isolated

Repetitive behaviours, interests, and activities:
- Stereotyped and repetitive motor mannerisms, inflexible adherence to nonfunctional routines or rituals
- particular ways of going about everyday activities

ASD is often associated with intellectual impairment or language impairment

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35
Q

How can Autism spectrum disorder be managed?

A

Early educational and behavioural interventions

SSRIs: reduce symptoms like repetitive stereotyped behaviour, anxiety, and aggression
Antipsychotic drugs: reduce symptoms like aggression, self-injury
Methylphenidate: for associated ADHD

Family support and counselling

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36
Q

What is Benign rolandic epilepsy?

A

form of childhood epilepsy that typically occurs between the age of 4 and 12 years

Features:
seizures characteristically occur at night
seizures are typically partial (e.g. paraesthesia affecting the face) but secondary generalisation may occur (i.e. parents may only report tonic-clonic movements)
the child is otherwise normal

Excellent prognosis; seizures usually stop by adolescence

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37
Q

What is biliary atresia?

A

obliteration or discontinuity within the extrahepatic biliary system, which results in an obstruction in the flow of bile = neonatal cholestasis in first few weeks of life

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38
Q

What are the 3 types of biliary atresia?

A

Type 1: obliteration of the common bile duct

Type 2a : obliteration of the common hepatic duct

Type 2b: obliteration of the common bile duct, cystic duct, and hepatic duct

Type 3: obliteration of the common bile duct, cystic duct, and hepatic duct up to the level of the porta hepatis (90% of cases)

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39
Q

Biliary atresia presents in the first few weeks of life with what symptoms and signs ?

A

Jaundice extending beyond the physiological two weeks
Dark urine and pale stools
Appetite and growth disturbance, (however, may be normal in some cases)
Hepatomegaly with splenomegaly
Cardiac murmurs if associated cardiac abnormalities present

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40
Q

How should biliary atresia be investigated?

A

Serum bilirubin : Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high

LFTs including serum bile acids and aminotransferases : usually raised but cannot differentiate causes of neonatal cholestasis

Serum alpha 1-antitrypsin: Deficiency may be a cause of neonatal cholestasis

Sweat chloride test: check for CF

Ultrasound of the biliary tree and liver: May show distension and tract abnormalities

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41
Q

How can biliary atresia be managed? Complications?

A

Surgical intervention is only definitive tx

Medical intervention includes antibiotic coverage and bile acid enhancers following surgery

Complications :
Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma

42
Q

What is Bronchiolitis? Offending pathogen? Presenting features?

A

acute bronchiolar inflammation

Usually RSV (respiratory syncytial virus)
other causes: mycoplasma, adenoviruses
may be secondary bacterial infection

coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles
feeding difficulties

43
Q

Give some signs of respiratory distress in a child

A

Raised respiratory rate
Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
Intercostal and subcostal recessions
Nasal flaring
Head bobbing
Tracheal tugging
Cyanosis (due to low oxygen saturation)
Abnormal airway noises

44
Q

Define wheezing, grunting and stridor

A

Wheezing is a whistling sound caused by narrowed airways, typically heard during expiration

Grunting is caused by exhaling with the glottis partially closed to increase positive end-expiratory pressure

Stridor is a high pitched inspiratory noise caused by obstruction of the upper airway, for example in croup

45
Q

In which patients is bronchiolitis more likely to be severe?

A

bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis

46
Q

When should 999 be called for a child with bronchiolitis?

A

child looks seriously unwell to a healthcare professional

apnoea- cessation of respiratory effort lasting more than 20 seconds, or shorter accompanied with bradycardia or cyanosis

severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute

central cyanosis

persistent oxygen saturation of less than 92% when breathing air

47
Q

How can bronchiolitis be investigated and managed?

A

immunofluorescence of nasopharyngeal secretions may show RSV

Management is largely supportive:
humidified oxygen is given via a head box
nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
suction is sometimes used for excessive upper airway secretions

48
Q

What options are available for ventilatory support in children?

A

High-flow humidified oxygen via tight nasal cannula (“Airvo” or “Optiflow”):
delivers air and oxygen continuously with some added pressure (“positive end-expiratory pressure” (PEEP)) to maintain the airway at the end of expiration

Continuous positive airway pressure (CPAP):
involves using a sealed nasal cannula that can deliver much higher and more controlled pressures

Intubation and ventilation

49
Q

What is palivizumab?

A

a monoclonal antibody that targets the respiratory syncytial virus

A monthly injection is given as prevention against bronchiolitis caused by RSV to high risk babies, such as ex-premature and those with congenital heart disease.

50
Q

What is bronchopulmonary dysplasia?

A

also known as Chronic lung disease of prematurity (CLDP)

It occurs in premature babies, typically before 28 weeks gestation, who suffer with respiratory distress syndrome and require oxygen therapy or intubation and ventilation at birth

Diagnosis is made based on chest xray changes and when the infant requires oxygen therapy after they reach 36 weeks gestational age.

51
Q

How can bronchopulmonary dysplasia (or CLDP) be prevented?

A

Giving corticosteroids (e.g. betamethasone) to mothers that show signs of premature labour at less than 36 weeks gestation

Once the neonate is born the risk of CLDP can be reduced by:

Using CPAP rather than intubation and ventilation when possible
Using caffeine to stimulate the respiratory effort
Not over-oxygenating with supplementary oxygen

52
Q

How can bronchopulmonary dysplasia (or CLDP) be managed?

A

formal sleep study to assess their oxygen saturations during sleep

Babies may be discharged from the neonatal unit on a low dose of oxygen to continue at home, via nasal cannula. They are followed up to wean the oxygen level over the first year of life.

Babies with CLDP require protection against respiratory syncytial virus (RSV) - monthly injections of a monoclonal antibody (palivizumab)

53
Q

Differntiate between Caput succedaneum and Cephalohaematoma

A

Both are swellings on the head of a newborn, more common following prolonged/ difficult deliveries
Managed conservatively

Caput succedaneum: soft tissue oedema
Present at birth
Typically forms over the vertex and crosses suture lines
Resolves within days

Cephalohaematoma: collection of blood between periosteum and skull
Typically develops several hours after birth
Most commonly in parietal region, doesn’t cross suture lines
May take months to resolve

54
Q

What is cerebral palsy?

A

disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain

Possible manifestations include:
abnormal tone in early infancy
hand preference below 18 months
delayed motor milestones
abnormal gait
feeding difficulties
learning difficulties

55
Q

Describe the gait that may be seen in cerebral palsy

A

hemiplegic or diplegic gait

this gait is caused by increased muscle tone and spasticity in the legs

the leg will be extended with plantar flexion of the feet and toes, meaning they have to swing the leg around in a large semicircle when moving their leg from behind them

56
Q

What may you see on examination of a patient with cerebral palsy?

A

signs of an upper motor neurone lesion

good muscle bulk, increased tone, brisk reflexes and slightly reduced power

look for athetoid movements that indicate extrapyramidal (basal ganglia) involvement

57
Q

What can cause cerebral palsy?

A

antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)

intrapartum (10%): birth asphyxia/trauma

postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma

58
Q

What are the different classifications of cerebral palsy?

A

spastic (70%)
hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons

dyskinetic
damage to the basal ganglia and the substantia nigra
athetoid movements and oro-motor problems

ataxic
caused by damage to the cerebellum with typical cerebellar signs

mixed

59
Q

Give some complications / associated conditions for cerebral palsy

A

Learning disability
Epilepsy
Kyphoscoliosis
Muscle contractures
Hearing and visual impairment
Gastro-oesophageal reflux

60
Q

What tx can be considered for cerebral palsy?

A

physiotherapy to strengthen muscles
OT
SLT
Dietetic support (some children require PEG tubes)

treatments for spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery and selective dorsal rhizotomy

anticonvulsants, analgesia as required.

61
Q

Chickenpox is caused by primary infection with varicella zoster virus. How does it present?

A

fever initially
itchy rash starting on head/trunk before spreading - macular then papular then vesicular
systemic upset is usually mild

infectivity = 4 days before rash, until 5 days after the rash first appeared

62
Q

How can chickenpox be managed?

A

keep cool, trim nails
calamine lotion
school exclusion: until lesions have crusted over (usually about 5 days after the onset of the rash)

immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG)
If chickenpox develops then IV aciclovir should be considered

63
Q

Complications of chickenpox?

A

Secondary bacterial infection of the lesions - NSAIDs may increase risk, group A strep may cause necrotising fasciitis

pneumonia
encephalitis (cerebellar involvement may be seen)
disseminated haemorrhagic chickenpox

64
Q

Spot diagnosis :
Microcephalic, small eyes
Cleft lip/palate
Polydactyly
Scalp lesions

A

Patau syndrome (trisomy 13)

65
Q

Spot diagnosis:

Micrognathia
Low-set ears
Rocker bottom feet
Overlapping of fingers

A

Edward’s syndrome (trisomy 18)

66
Q

Spot diagnosis :

Learning difficulties
Macrocephaly
Long face
Large ears
Macro-orchidism

A

Fragile X

67
Q

Spot diagnosis :

Webbed neck
Pectus excavatum
Short stature
Pulmonary stenosis

A

Noonan syndrome

68
Q

Spot diagnosis:

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

A

Pierre-Robin syndrome

69
Q

Spot diagnosis:

Hypotonia
Hypogonadism
Obesity

A

Prader-Willi syndrome

70
Q

Spot diagnosis :

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

A

William’s syndrome

71
Q

Spot diagnosis :

Characteristic cry (hence the name) due to larynx and neurological problems
Feeding difficulties and poor weight gain
Learning difficulties
Microcephaly and micrognathism
Hypertelorism

A

Cri du chat syndrome (chromosome 5p deletion syndrome)

72
Q

How do cleft lip and cleft palate form?

A

polygenic inheritance
maternal antiepileptic use increases risk
cleft lip results from failure of the fronto-nasal and maxillary processes to fuse
cleft palate results from failure of the palatine processes and the nasal septum to fuse

73
Q

How can feeding and speech be improved in children with cleft lip / palate?

What problems can cleft palate cause?

A

feeding: orthodontic devices may be helpful
speech: with speech therapy 75% of children develop normal speech
increased risk of otitis media for cleft palate babies

74
Q

How are cleft lip and palate managed?

A

cleft lip is repaired earlier than cleft palate, with practices varying from repair in the first week of life to three months
cleft palates are typically repaired between 6-12 months of age

75
Q

Coeliac disease is caused by sensitivity to gluten, with repeated exposure leading to villous atrophy which in turn causes malabsorption. Children normally present before the age of 3 years.

What features may the present with?

A

Features may coincide with the introduction of cereals (i.e. gluten)
failure to thrive
diarrhoea
abdominal distension
older children may present with anaemia
many cases are not diagnosed to adulthood

76
Q

What other conditions are associated with coealic disease?

A

Down’s syndrome
autoimmune thyroid disease
IDDM

77
Q

What is dermatitis herpetiformis?

A

an itchy, blistering skin rash, typically on the abdomen, caused by coeliac disease

78
Q

How is coeliac diagnosed?

A

jejunal biopsy showing subtotal villous atrophy and crypt hyperplasia

First line blood tests:
Total IgA levels (to exclude IgA deficiency)
Anti-tissue transglutaminase antibodies (anti-TTG)
(anti-endomysial and anti-gliadin antibodies are also useful)

79
Q

Complications of coeliac disease?

A

Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL)
Non-Hodgkin lymphoma
Small bowel adenocarcinoma

80
Q

What is Congenital diaphragmatic hernia (CDH)?

A

the herniation of abdominal viscera into the chest cavity due to incomplete formation of the diaphragm

can result in pulmonary hypoplasia and hypertension which causes respiratory distress shortly after birth

81
Q

Give some acyanotic congenital heart diseases

A

ventricular septal defects (VSD)
atrial septal defect (ASD)
patent ductus arteriosus (PDA)
coarctation of the aorta
aortic valve stenosis

82
Q

Give some cyanotic congenital heart diseases

A

tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia

83
Q

What is the most common congenital infection in the UK?

A

Cytomegalovirus

84
Q

What are the characteristic features of congenital rubella?

A

Sensorineural deafness
Congenital cataracts
Congenital heart disease (e.g. patent ductus arteriosus)
Glaucoma

85
Q

What are the characteristic features of congenital toxoplasmosis?

A

Cerebral calcification
Chorioretinitis
Hydrocephalus

86
Q

What are the characteristic features of congenital CMV?

A

Low birth weight
Purpuric skin lesions
Sensorineural deafness
Microcephaly

87
Q

What are the causes of constipation in children?

A

Idiopathic - most common
dehydration
low-fibre diet
medications: e.g. Opiates
anal fissure
over-enthusiastic potty training
hypothyroidism
Hirschsprung’s disease
hypercalcaemia
learning disabilities

88
Q

What red flags might suggest an underlying condition as opposed to idiopathic constipation?

A

Reported from birth or first few weeks of life

Passage of meconium > 48 hours

‘Ribbon’ stools

Abdominal distension

Faltering growth is an amber flag

Previously unknown or undiagnosed weakness in legs, locomotor delay

Signs of maltreatment

89
Q

Prior to starting treatment for constipation, the child needs to be assessed for faecal impaction. Factors which suggest faecal impaction include:

A

symptoms of severe constipation
overflow soiling
faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)

90
Q

How can children with constipation be managed?

A

If faecal impaction is present
polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment

Can add a stimulant laxative after 2 weeks if needed

consider regular toileting and non-punitive behavioural interventions

consider asking the Health Visitor or Paediatric Continence Advisor to help support the parents

91
Q

How can constipation in an infant be managed?

A

Infants not yet weaned (usually < 6 months)
bottle-fed infants: give extra water in between feeds. Try gentle abdominal massage and bicycling the infant’s legs
breast-fed infants: constipation is unusual and organic causes should be considered

Infants who have or are being weaned
offer extra water, diluted fruit juice and fruits
if not effective consider adding lactulose

92
Q

Give some features of Cow’s milk protein intolerance/allergy (CMPI/CMPA)

A

regurgitation and vomiting
diarrhoea
urticaria, atopic eczema
‘colic’ symptoms: irritability, crying
wheeze, chronic cough
rarely angioedema and anaphylaxis

93
Q

How can cows milk allergy be investigated and managed?

A

Diagnosis is often clinical (e.g. improvement with cow’s milk protein elimination)

Ix:
skin prick/patch testing
total IgE and specific IgE (RAST) for cow’s milk protein

Mx:

Management if formula-fed =
extensive hydrolysed formula (eHF) milk is the first-line replacement formula

Management if breastfed =
continue breastfeeding
eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers

94
Q

What is the prognosis for children with non-IgE mediated intolerance to cows milk?

A

Most children with non-IgE-mediated cow’s milk protein allergy will be milk tolerant by 3 years of age

95
Q

What is Croup?

A

also known as laryngotracheitis

URTI characterised by stridor which is caused by a combination of laryngeal oedema and secretions

Usually caused by parainfluenza virus

typically affects children aged 6 months to 2 years

96
Q

Presenting features of croup?

A

stridor
barking cough (worse at night)
fever
coryzal symptoms

97
Q

When should children be admitted with croup?

A

Moderate / severe
< 6 months of age
known upper airway abnormalities (e.g. Laryngomalacia, Down’s syndrome)
uncertainty about diagnosis (important differentials include acute epiglottitis, bacterial tracheitis, peritonsillar abscess and foreign body inhalation)

98
Q

How can croup be managed?

A

single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity
high-flow oxygen
nebulised adrenaline

99
Q

Central cyanosis in the neonatal period can be recognised clinically when the concentration of reduced haemoglobin in the blood exceeds 5g/dl. How can you distinguish between cardiac and non-cardiac causes?

A

The nitrogen washout test

The infant is given 100% oxygen for ten minutes after which arterial blood gases are taken. A pO2 of less than 15 kPa indicates cyanotic congenital heart disease

100
Q

Initial management of suspected cyanotic congenital heart disease?

A

supportive care

prostaglandin E1 e.g. alprostadil
used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect
this can act as a holding measure until a definite diagnosis is made and surgical correction performed

101
Q

What is Acrocyanosis?

A

often seen in healthy newborns and refers to the peripheral cyanosis around the mouth and the extremities (hands and feet)

occurs immediately after birth in healthy infants. It is a common finding and may persist for 24 to 48 hours.