Paediatrics 2 Flashcards

1
Q

Autism clinical features

A
  • Social communication impairment and repetitive behaviour can be present before 2-3 years of age
  • Often associated with intellectual impairment or language impairment i.e. monotonous tone of voice, interpret speech literally
  • Attention deficit hyperactivity disorder (35%) and epilepsy (18%) are also commonly seen in children with ASD.
  • ASD is also associated with a higher head circumference to the brain volume ratio.
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2
Q

Autism behaviour

A
  • Repetitive behaviour, interests and activities= stereotyped and repetitive motor mannerisms, inflexible adherence to non-functional routines or rituals. Children are noted to have a particular way of doing everyday activity. Narrow interests i.e. trains
  • Impaired social communication and interaction= children frequently play alone and uninterested in being with other children. 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
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3
Q

Autism management

A
  • Involves educational and behavioural management, medical therapy and family counselling
  • Goal is to increase functional independence and quality if life through: Learning and development, improved social skills and improved communication
  • Applied behavioural analysis: positive behaviours are encouraged and negative behaviours are ignored
  • ASD preschool programme
  • Aid to families

Family support and counselling: parental education on interaction with the child and acceptance of his/her behaviour

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4
Q

Autism pharmacological interventions

A

no consistent evidence demonstrating medication mediated improvements in social communication

  • SSRI’s: help reduce symptoms like repetitive stereotypes behaviour, anxiety and aggression
  • Antipsychotic drugs: useful to reduce symptoms like aggression, self-injury
  • Methylphenidate: for ADHD
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5
Q

Symptoms of biliary atresia

A
  • Prolonged jaundice (i.e., jaundice persisting beyond 14 days of life)
  • Signs of biliary obstruction such as dark urine and pale or chalky white stool
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6
Q

Investigations for biliary atresia

A
  • Blood tests
  • Hepatic scintigraphy (Technetium-99m scan): The liver will take up the isotope but there will be poor excretion into the bowel, indicating destroyed bile ducts.
  • Abdominal ultrasound: This may reveal echogenic fibrosis.
  • Cholangiography: This is the definitive diagnostic test, which will fail to show normal architecture of the biliary tree, confirming biliary atresia.
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7
Q

Management of biliary atresia

A

Hepatoportoenterostomy (Kasai procedure): This surgery creates a new pathway from the liver to the gut to bypass the fibrosed bile ducts.

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8
Q

Cause of bronchiectasis in paediatrics

A
  • CF: most common
  • Chronic infection: s.pneumonia, s.aureus
  • Immunodeficiency: agammaglobulinaemia, HIV, ataxic telangiectasia
  • Primary ciliary dyskinesia: autosomal recessive, loss of bronchial cilia
  • Youngs syndrome
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9
Q

Symptoms of bronchiectasis

A
  • Purulent sputum expectoration
  • Chest pain
  • Wheeze
  • Breathlessness on exertion
  • Haemoptysis
  • Recurrent or persistent infections of the lower respiratory tract
  • Signs: finger clubbing, wheeze and inspiratory crackles
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10
Q

Investigations for bronchiectasis

A
  • CXR
  • HRCT: gold standard
  • Bronchoscopy: after CT
  • Chloride sweat test: for CF
  • Spirometry
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11
Q

Management of bronchiectasis

A
  • Chest physiotherapy
  • antibiotics for exacerbations
  • Bronchodilators if wheeze
  • Most common exacerbations: H.influenza, S.pneumoniae
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12
Q

Complications of bronchiectasis

A
  • Recurrent infection
  • Life-threatening haemoptysis
  • Lung abscess
  • Pneumothorax
  • Poor growth and development
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13
Q

Bronchiolitis key features

A
  • Common in babies and in young children below 2 years of age
  • Usually caused by viruses (mainly RSV), other causes: mycoplasma, adenoviruses
  • May be secondary to a bacterial infection
  • More serious if bronchopulmonary dysplasia i.e. premature, congenital heart disease or cystic fibrosis
  • Palivizumab (RSV vaccine ) is offered to high risk babies ( eg congenital heart disease, babies on home oxygen)
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14
Q

Bronchiolitis high risk babies

A

more likely to require admission to hospital:

  • Premature babies (< 32 weeks)
  • Chronic lung disease (home oxygen)
  • Congenital heart disease
  • Young babies (less than 12 weeks old)
  • Neuromuscular disease
  • Consider admission if there are social concerns for example parents with learning difficulties, young parents with poor support, remote location and difficulty accessing care
  • These children are given the palivizumab injections in winter
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15
Q

Bronchiolitis symptoms

A
  • Coryzal features (including mild fever) precede:
  • Dry cough
  • Increasing breathlessness
  • Wheezing, fine inspiratory crackles
  • Feeding difficulties associated with increasing dyspnoea and often the reason for hospital admissions
  • Increased work of breathing: tachypnoea, nasal flaring, head bobbing, tracheal tug, intercostal/sternal recessions and abdominal breathing
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16
Q

Bronchiolitis: NICE recommends immediate referral (usually by 999 ambulance) if they have any of the following:

A
  • apnoea (observed or reported)
  • child looks seriously unwell to a healthcare professional
  • 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.
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17
Q

NICE: NICE recommend that clinicians ‘consider’ referring to hospital if any of the following apply:

A
  • a respiratory rate of over 60 breaths/minute
  • difficulty with breastfeeding or inadequate oral fluid intake (50-75% of usual volume ‘taking account of risk factors and using clinical judgement’)
  • clinical dehydration.
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18
Q

Bronchiolitis: investigations and management

A
  • Investigations: immunofluorescence of nasopharyngeal secretions may show RSV
  • Diagnosis is primarily clinical can use CXR
  • Management is largely supportive
  • Humidified oxygen is given via a head box and is typically recommended if the oxygen saturations are persistently < 92%
  • Nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
  • Suction is sometimes used for excessive upper airway secretions
  • Severe cases: CPAP, endotracheal intubation and ventilation
  • Antiviral therapy: Ribavirin is used in severe cases
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19
Q

Bronchiolitis: discharge criteria

A
  • Oxygen saturation maintained at >92% for 4 hours including a period of sleep
  • Adequate oral intake (75% of normal)
  • If babies are seen at the beginning of their illness inform the parents that they need to be carefully observed as they often get worse (day 3) before they get better
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20
Q

Bronchiolitis obliterans

A
  • A rare chronic complication of bronchiolitis, called popcorn lung
  • Lungs are damaged by infection causing overactive cellular repair causing scar tissue to build
  • Scarring and narrowing of bronchioles leading to respiratory failure
  • Also occurs with lung transplant recipients
  • Supportive treatment with immunosuppressive drugs i.e. Tacrolimus, cyclosporin
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21
Q

When to admit a child with candidiasis

A
  • Widespread systemic illness
  • Oesophageal candidiasis (difficulty or pain swallowing)
22
Q

Symptoms of candidiasis

A
  • White or creamy patches on the tongue, inner cheek, gum or tonsils
  • Painful, causes discomfort while eating or drinking
  • Very common in babies
23
Q

Management of candidiasis

A
  • Miconazole oral gel: first line if >4 months
  • Nystatin suspension: <4 months
24
Q

Paediatric BLS algorithm

A
  • Unresponsive → call for help (2222)
  • Open airway: head tilt, chin lift
  • Assess breathing
  • Give 5 rescue breaths
  • Assess breathing
  • Give 15 chest compressions to 2 rescue breaths
25
Q

How to open airway paediatrics

A
  • Infant: neutral position, hold hard parts of face
  • Small child: sniffing the morning air (head tilt and chin lift)
  • Older child: extended neck position with head tilt chin lift
26
Q

Paediatric chest compressions

A
  • Infant: either 2 fingers or both thumb gripping across the chest
  • Child: 1 hand
27
Q

Paediatric chocking algorithm

A
  • Suspected foreign body obstruction
  • Shout for help
  • If they can cough effectively encourage them to do so
  • If they cant cough call the resus team
  • If child is unconscious start CPR
  • If not unconscious do up to 5 back blows and 5 abdominal thrusts. Then continue till help arrives
28
Q

Difference in chocking algorithm with infants and children

A
  • Infant: 5 back blows and 5 chest thrusts
  • Child: 5 back blows and 5 abdominal thrusts
  • Back blows: in infant hold over your forearm and check mouth after each blow. In child lean forward and check mouth each time
  • Chest/abdominal thrusts: in infants hold on their back with their head facing down, use two fingers in a scooping motion. In child use two fists whilst leaning forward
29
Q

Airway insertion paediatrics

A
  • Oropharyngeal < 8yrs – Follow the direction of the airway downwards to avoid damaging soft palate. Use tongue depressor or laryngoscope to move tongue out of the way.
  • Oropharyngeal >8 yrs – insert as would in adult, so upside down and then twist.
  • Nasopharyngeal: sizing is tip of the nose to the tragus. Insert in one nostril and follow the direction of the airway downwards. Dont insert if basal skull fracture
30
Q

Peri-orbital cellulitis

A
  • Primarily affects children and adolescents
  • Can have sinus involvement
  • Organosms: S.pneumoniae, H.influenzae
  • Features: eyelid oedema and erythema
  • Orbital signs: proptosis, ophthalmoplegia, decreased visual acuity, loss of red vision
  • Treat: broad spectrum antibiotics
31
Q

Cerebral palsy and HIE

A

A group of permanent movement disorder that occur due to damage to the childs CNS involved in motor control. Lesions are non-progressive I.e. it does not get worse

32
Q

Cerebral palsy and HIE causes

A
  • Antenatal: Hypoxic-ischaemic encephalopathy, infection
  • Post-natal: Meningitis, Trauma, Haemorrhage, Medication toxicity, Kernicterus
  • Idiopathic
33
Q

Cerebral palsy classification: spastic

A
  • 90% have some spastic features
  • damage to pyramidal pathways ( pyramidal weakness)
  • General features: increased tone and reflexes, clasp knife, flexed hip and elbow
  • Scissor gait
  • May be monoplegic, diplegic, hemiplegic
34
Q

Cerebral palsy classification: Dyskinetic/athetoid

A
  • Damage to the basal ganglia pathways
  • Choreiform movements
  • Can exhibit signs of Parkinsonism
35
Q

Cerebral palsy: Ataxic

A
  • Damage to cerebellar pathways
  • Uncoordinated movements
  • Signs of cerebellar lesions
36
Q

Patterns of spastic cerebral palsy

A
  • Monoplegia: one limb affected
  • Hemiplegia: one side of the body affected
  • Diplegia: four limbs are affects, but mostly the legs
  • Quadriplegia: four limbs are affected more severely, often with seizures, speech disturbance and other impairments
37
Q

Cerebral palsy investigations

A
  • MRI head: visualise lesion
  • Genetic testing: for different diagnosis
38
Q

Cerebral palsy complications

A
  • Injuries from impaired balance/coordination
  • Aspiration pneumonias from impaired swallowing
  • Muscle wasting
  • Scoliosis and other MSK deformities from impaired posture and muscle control
39
Q

Cerebral palsy management: MDT

A
  • Physiotherapy to help with movement and strength exercises
  • Occupational therapy may help with mobility aids, home adjustments and devices such as orthotics
  • Speech and language therapy for swallowing assessments
  • Dieticians if there are concerns regarding low intake due to swallowing difficulties
40
Q

Cerebral palsy management: medical and surgery

A
  • Medical: Baclofen for spasm, Botulinum toxin type A injections used for spasticity and contractures.. Diazepam for pain. Hyoscine hydrobromide or glycopyronium bromide for excess drooling. Anti-epileptics for seizures
  • Surgical management: Orthopredic surgery for MSK deformity/injuries/tendon release. General surgery if a PEG tube needs fitting
41
Q

Cerebral palsy: possible manifestations

A
  • abnormal tone early infancy i.e. floppy or stiffness
  • delayed motor milestones: not sitting by 8 months, not walking by 18 months, hand preference before 12 months
  • abnormal gait
  • feeding difficulties i.e. chocking, dysphagia
  • Persistent toe walking
  • Non-motor problems i.e. learning difficulties (60%), epilepsy (30%), squints (30%), hearing impairment (20%)
42
Q

Cerebral palsy diagnosis and complications

A

Cerebral palsy is a clinical diagnosis but no diagnostic tests, an MRI brain can be requested to rule out differentials.

Complications
- Problems with feeding and aspiration, Drooling
- Constipation
- Visual and hearing impairment, sleep disturbances
- Epilepsy
- Learning disability, Speech difficulty
- Osteopenia and osteoporosis (especially if non-mobile)

43
Q

Key symptoms of cerebral palsy

A
  • Failure to meet milestones
  • Increased or decreased tone, generally or in specific limbs
  • Hand preference below 18 months is a key sign to remember for exams
  • Problems with coordination, speech or walking
  • Feeding or swallowing problems
  • Learning difficulties
44
Q

Causes of CKD in children

A
  • An AKI that doesnt improve
  • Chronic, severe high blood pressure
  • Frequent dehydration
  • Glomerulonephritis
  • PCKD
  • Kidney malformation at birth
  • Lupus
  • repeated UTI’s
  • Kidney stones or tumours
45
Q

Coeliac disease pathophysiology

A

Sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Children normally present before the age of 3 years, following the introduction of cereals into the diet. Strongly associated HLA-DQ2and HLA-DQ8. Associated with type 1 diabetes

46
Q

Coeliac disease symptoms

A
  • failure to thrive: fatigue, weight loss
  • diarrhoea
  • Nausea and vomiting, Steatorrhoea
  • abdominal distension and pain
  • older children may present with anaemia
  • many cases are not diagnosed to adulthood
  • Dermatological: dermatitis herpetiformis (itchy blistering rash on the abdomen
47
Q

Coeliac disease diagnosis

A
  • Investigations must be done when patient is still consuming gluten
  • Gold standard: OGD and duodenal/jejunal biopsy
  • Histology: sub-total villous atrophy, crypt hyperplasia and intra-epithelial lymphocytes
  • anti-endomysial and anti-gliadin antibodies are useful screening tests
  • First line: Anti-TTG IgA antibodies and IgA levels
  • Test everyone with T1D for coeliac
48
Q

Coeliac disease management and complications

A

Management: life long gluten free diet, regular monitoring

Complications
- Anaemia (secondary to iron, B1 or folate deficiency)
- Hyposplenism (and therefore a susceptibility to encapsulated organisms)
- Osteoporosis (a DEXA scan may be required)
- Enteropathy-associated T cell lymphoma (EATL; a rare type of non-Hodgkin lymphoma)

49
Q

Acyanotic cardiac lesions

A
  • Ventricular septal defects (VSD)
  • Atrial septal defects (ASD)
  • Patent ductus arteriosis (PDA)
50
Q

Features of acyanotic cardiac lesions

A
  • Left to right shunting, mixing of oxygenated blood with deoxygenated blood
  • Increased pulmonary blood flow → risk of pulmonary hypertension and untreated acyanotic heart disease can lead to Eisenmenger syndrome
  • Lesions that are above the level of the nipple usually give rise to ejection systolic murmurs while lesions below the level of the nipple typically cause pan systolic murmurs