1
Q
what are the types of ADHD?
A
- inattention: not listening, distractible, losing things
- hyperactive-impulsive: restless, reckless, energy, impatient
- combined: most common
2
Q
what are some RF for ADHD?
A
genetic, low birth weights, maternal smoking, preterm delivery, epilepsy, alcohol in pregnancy, iron deficiency etc, males more at risk, FH, social deprivation
3
Q
what features will prompt a diagnosis of ADHD?
*DSM-V
A
- inattention - distracted by stimuli, forgetful in daily activities, difficulty sustaining attention
- hyperactivity - fidgets, talks excessively, driven by motor
- impulsivity - difficulty waiting turn, bursts out answers before questions completed
4
Q
what are some differentials for ADHD?
A
- auditory processing disorder
- oppositional defiant disorder or conduct disorders
- depression
- anxiety
- ASD
5
Q
how is ADHD investigated?
A
- questionnaires to gather info like conner’s
- school observation to observe functioning and interaction, academic attainment assessed
- info from school, home, childminder etc to show presence in more than one setting
6
Q
how is ADHD managed?
A
- behavioural strategies, parent education, CBT, social skills training, teacher training
- medication like Methylphenidate
7
Q
how is methylphenidate monitored?
A
- height and weight as potential stunting with methylphenidate
- CVS: BP, tachycardia monitor
- tics: reduce dose
- seizures, sleep, sexual dysfunction etc
8
Q
what is ASD?
A
neurodevelopmental disorder that affects person’s social interaction, communication and behaviour, diagnosis in childhood with key symptoms before age 3
9
Q
what are some RF of developing ASD?
A
- genetics: fragile X syndrome, Down’s syndrome,
- siblings with ASD
- parental age over 40
- sodium valproate in pregnancy
- rubella infection in mother
- obstetric complications like hypoxia
10
Q
what are some key points in a hx that may suggest ASD?
A
- persistent difficulties in social interaction and communication: few social gestures, lack of eye contact etc, distorted speech, echolalia
- stereotypical, rigid, repetitive behaviours
- resistance to change or restricted interest
- sensory problems involving food
- self harm
11
Q
what are some differentials to consider for ASD?
A
- learning difficulties - can co-exist
- attachment disorders
- Rett’s syndrome - speech delay and repetitive hand movements in girls
- schizophrenia - odd behaviours, but rare in children
- specific language disorders
12
Q
how is ASD investigated?
A
- clinical diagnosis
- main focus is to gather information to support diagnosis from different environments
- report about child’s function at school and school observation
- MDT meeting with parents and teachers - MDT has educational psychologist, speech therapist, community paediatrician, child psychiatrist
13
Q
how is ASD managed?
A
*diagnosis by specialist by age 3
- MDT care
- family support, self help groups, psychoeducation, special schooling
- stress reduction, env changes
- melatonin for sleep, manage co-morbidities
14
Q
what are some causes of cerebral palsy?
*think prenatal, perinatal, postnatal
A
- prenatal causes - APH (with hypoxia), radiation, alcohol, rubella, HIV, CMV, rhesus disease
- perinatal - prematurity, birth asphyxia, hypoglycaemia
- postnatal - trauma, hypoxia, meningoencephalitis, cerebral vein thrombosis, severe neonatal jaundice
15
Q
what are some types of CP?
A
spastic - hypertonia and reduced function as a result of upper motor neurone damage
dyskinetic - problems controlling muscle tone
ataxic - problems with co-ordinated movement as cerebellum damaged
mixed
16
Q
how might CP present if not diagnosed earlier?
A
- weakness, paralysis, increased tone, coordination problems
- premature handedness or other motor asymmetry - ie hand preference, esp before 18m
- delayed milestones, language/ speech/ learning difficulties
- swallowing and feeding problems
17
Q
what signs may be present on examination of CP?
A
- hemiplegic/ diplegic gait - upper motor lesion
- broad based gait or ataxic gait - cerebellar
- high steppage gait - foot drop or lower motor lesion
- waddling gait - pelvic muscle weakness/ myopathy
- antalgic gait - localised pain
18
Q
what are some complications associated with CP?
A
learning disability, epilepsy, kyphoscoliosis, muscle contractures, hearing and visual impairments, GORD
19
Q
how is CP managed?
A
*MDT
- physio: strengthen and stretch muscles, maximise function
- OT: ADL, assistance
- SALT
- dieticians
- Ortho: to release contractures, lengthen tendons etc
- medications
- social workers, charities etc
20
Q
what is the role of medication in CP?
A
- muscle relaxants - baclofen for spasticity, contactures
- anti-epileptic for seizures
- glycopyrronium bromide for excessive drooling
21
Q
what is the pathophysiology of down’s syndrome ?
A
trisomy 21 where extra copies of chromosome 21 in each cell, so instead of the normal 46 there are 47 chromosomes occurring sporadically
*The three main genetic mechanisms responsible for Down syndrome are gamete non-disjunction, Robertsonian translocation, and mosaicism
22
Q
what is the most prominent RF for DS?
A
incidence of Down syndrome increases with maternal age (35+), especially for cases resulting from gamete non-disjunction
23
Q
what is the screening process for DS?
A
the combined test is now standard
*these tests should be done between 11 - 13+6 weeks
nuchal translucency measurement + serum B-HCG + pregnancy-associated plasma protein A (PAPP-A)
24
Q
what results are suggestive of DS?
A
Down’s syndrome is suggested by ↑ HCG, ↓ PAPP-A, thickened nuchal translucency
25
what are some physical features of DS?
upward-slanting palpebral fissures
epicanthal folds
protruding tongue
small low-set ears with adherent earlobes
hypoplastic nasal bridge - broad and flat
small oral cavity, and a single transverse palmar crease
26
what are some complications caused by DS?
- visual: congenital cataracts, infantile glaucoma
- hearing: conductive HL
- ENT: small upper airway so infection risk, glue ear
- CVS: AVSD
- resp: recurrent infections, impaired immunity
- MSK: hypotonia, early feeding difficulty
- growth: poor, short
- endocrine: hypothyroidism
- haem: myeloproliferative, increased AML risk
- neuro: alzheimers
27
how is DS managed?
- MDT coordinated by community or neurodisability paediatrician
- personal child health record as additional to red book to guide care
- speciality input for comorbidities - cardio, ENT, resp and surgeons
- aim - treat comorbidities, promote health, development and reduce disability or functional limitation
- routine schedule advised by DS medical interest group to identify possible growth delay, resp and cardiac problems etc
- genetic counselling for families for subsequent pregnancies, karyotyping analysis
28
how is DS investigated?
- antenatal screening
- early counselling with senior paediatrician and midwife
- blood test - QF-PCR then G banded analysis, FBC and blood film
- newborn eye assessment
- universal newborn hearing screen
- Gutherie test - blood sport on day 5 for congenital hypothyroidism
- ECG and echo
29
how do you differentiate between BN & AN?
- normal weight or overweight
- less endocrine
- strong food cravings
- recurrent binging
- compensatory behaviours definitely
30
how does AN present?
- self induced weight loss resulting in low BMI, <17.5
- distorted perception of her body which increases with weight loss
- restricting food intake to lose weight
- amenorrhoea
- preoccupation with food - cooking for others and reading cookery books etc
- poor insight - denying hunger, claiming health
- changes in mood - anxiety and depression
31
how is BN presented?
- use of purging methods
- PMH of being overweight
- recent major weight loss
32
how might you detect AN on examination?
- lanugo hairs
- hypokalaemia signs
- hypotension
- slow reflexes
- reduced peripheral circulation
- bradycardia
- ankle oedema with low proteins
33
how might you detect BN on examination?
- hypokalaemia
- alkalosis due to vomiting HCL
- erosion of teeth
- swollen parotid glands
- mouth ulcers
- GORD and irritation
- Russel’s sign knuckle calluses
34
how might you investigate ED?
- FBC - normocytic, normochromic anaemia, low WCC, platelets
- U&E - low K+ due to vomiting, low Na+ and K+ from laxatives, low phosphate and magnesium
- LFT - loss of proteins
- lipids - hypercholestrolaemia
- hormones - LH, FSH, Oestridiol TFT, cortisol
- glucose - impaired tolerance as high
- VBG
- DEXA - from ED team
- ECG - CVS abn. if low electrolytes
35
how is AN managed?
- risk assessment is vital
- psychological treatment 6m (CBT-ED, family therapy, MANTRA)
- aim for controlled weight gain
- refeeding syndrome risk
- hospitalisation if BMI<14 and psychiatric
- medications for complications and depression
- self help groups etc
36
how is BN managed?
- antidepressants, treat complications, treat co-morbids
- psychoeducation, interpersonal psychotherapy, family therapy
- food diary, self help
- risk assessment
- 50% fully recover compared to 20% in AN
37
what are adult RF for NAI?
mental illness, PND, lack of social support, drugs, own child abuse, alcohol misuse, learning disability, criminal activity, financial difficulties
38
what are some child RF for NAI?
being unwanted, unable to fulfill expectations, crying, under 4, disability, ill health
39
how might physical abuse present
- mechanism of injury not compatible with injury sustained
- child's developmental stage inconsistent with injury presented
- sustaining significant injury with little to no explanation
- inconsistent histories
- delay in presenting to health care providers
- recurrent injuries
- parents reaction not appropriate to situation - too concerned, aggressive, elusive, vague
40
how might neglect present?
- unimmunised
- failure to attend appointments
- poor compliance with medications
- faltering growth
- obesity
- poor school attendance
41
how might emotional abuse present?
- infant - developmental delay, poor sleep, feeding difficulties, persistent crying, irritable, apathetic
- toddler - difficult/ violent behaviour, delayed social and language skills
- school - poor attendance, truancy, antisocial behaviour, academic failure
- adolescent - depression, self harm, relationship difficulties, substance abuse, criminal activity, ED, aggressive behaviours
42
how might sexual abuse present?
- soiling, bowel problems
- enuresis
- behavioural difficulties
- allegation by child
- pregnancy
- STI
- ano-genital injury
- unexplained vaginal, rectal bleeding
43
what features on examination may lead you to suspect physical abuse?
- burns
- abdominal injury
- bruises in back, face, buttocks (away from bony prominences) - outlines maybe seen of belt or hand
- fractures especially if less than 18m - consider age, location as common sites rib, vertebrae and metaphyseal, type of fracture and multiple #
- head injury under 6m result of shaking as may cause small vessel rupture leading to subdural haemorrhage
- subconjuctival haemorrhage, apnoea, poor feeding, convulsions, signs of high ICP etc
44
what are some differentials for NAI?
bleeding disorder, birth marks, infection // # birth injury, infection, osteogenesis imperfecta, vitamin D deficiency
45
how are NAI investigated?
- bruising - coagulation screen, FBC
- #- full skeletal survey, CT scan, bone biochemistry
- suspected abuse in less than 2 year old - full skeletal survey, CT head, ophthalmological examination, coagulation screen
46
how is NAI managed?
- document clearly, seek advice, contact safeguarding, keep child safe
- respond to disclosure - try not to look shocked, let child know you believe them, tell them they are not in trouble, listen to what they have to say, don’t ask leading questions, don’t make promises you cannot keep, be honest, inform senior
47
what defines a developmental delay?
2 or more of the following 4 developmental areas
- gross motor
- fine motor
- speech and language
- social and emotional
*Global delay may suggest downs syndrome, fragile X, fetal alcohol syndrome, metabolic disorders
48
what causes developmental delays?
- neurological: congenital + acquired (HIE)
- infection: rubella, CMV, herpes, HIV
- neuromuscular
- hypothyroidism
- genetic: downs syndrome
- pervasive developmental disorders: autism
- metabolic: phenylketonuria, Krabbe’s
- prematurity
- idiopathic
49
when might you suspect a developmental delay?
- child not hitting milestones
- referral from health visitor as part of routine checks for development
- concerns raised by early education setting or school
- as part of follow up if child was premature etc so high risk of developmental delay
- 18m old not walking yet or generalised delay like 2y/o not able to imitate scribbles
- REFER TO PAEDIATRIC SPECIALIST
50
what are some red flags for developmental delays?
- social: not smiling by 10w
- gross motor: Not sitting unsupported by 12 months, Not walking by 18 months
- fine motor: Showing hand preference before 12 months of age
- speech and language: Not knowing 2-6 words by 18 months
51
how are developmental delays investigated?
- FBC
- U&E
- CK
- TFT
- LFT
- Vit D
- Hearing test
*2nd line karyotyping, DNA analysis, detailed metabolic screens, MRI and EEG
52
how are developmental delays managed?
- community paediatrician to perform detailed developmental assessment and holistic examination of child and family
- griffiths scales of child development or schedule of growing skills used to assess developmental domains
- multi-disciplinary care for child and family
- speech and language therapists
- portage practitioners
- orthoptics
- hospital paediatricians
- if reversible cause treat this!!
Y4 Paediatrics
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