1- Community Paediatrics Flashcards
ADHD background
People with ADHD are at the extreme ends of hyperactivity and inability to concentrate (attention deficit).
- Affects persons ability to carry out everyday tasks, develop normal skills and perform well in school
ADHD: management
- Detailed assessment by specialist
- Parental and child education essential
- Healthy diet and exercise can offer significant improvement to symptoms
- Medication (only for severe cases)- CENTRAL NERVOUS STIMULANTS (contrary to common belief)
ADHD: Causes/risk factors
Not fully understood
- Genetics (does run in families)
- Premature babies or low birthweight
- Epilepsy
- Brain damage either in womb or later in life
ADHD: 3 core features
Inattention:
- Short attention span for age (difficulty sustaining attention)
- Difficulty listening to others
- Difficulty attending to details
- Easily distracted
- Forgetfulness
- Poor organizational skills for age
- Poor study skills for age
Impulsivity:
- Often interrupts others
- Has difficulty waiting for his or her turn in school and/or social games
- Tends to blurt out answers instead of waiting to be called upon
- Takes frequent risks, and often without thinking before acting
Hyperactivity:
- Seems to be in constant motion; runs or climbs, at times with no apparent goal except motion
- Has difficulty remaining in his/her seat even when it is expected
- Fidgets with hands or squirms when in his or her seat; fidgeting excessively
- Talks excessively
- Has difficulty engaging in quiet activities
- Loses or forgets things repeatedly and often
- Inability to stay on task; shifts from one task to another without bringing any to completion
ADHD: presentation
Features should be consistent across various setting e.g. only displaying features at school and being well behaved at home – environmental problem
* Very short attention span
* Quickly moving from one activity to another
* Quickly losing interest in a task and not being able to persist with challenging tasks
* Constantly moving or fidgeting
* Impulsive behaviour
* Disruptive or rule breaking
ADHD: medication
- Methylphenidate (Ritalin)- first line drug
- Dexamphetamine
- Atomoxetine
MOA
Stimulant medication such as methylphenidate. These medicines have some activity in the frontal lobe thus increasing executive function, attention, and reducing impulsivity.
ASD: background
- A spectrum which causes deficits in social interaction, communication and flexible behaviour
- Autism spectrum replaced the differentiation between Aspergers syndrome and autistic disorder and grouped them into one spectrum disorder
- Big range
- One end patients have normal intelligence and ability to function in everyday life but displaying difficulties when reading emotions and responding to others (Asperger’s)
- On the other end, patients can be severely affected and unable to function in normal environments
ASD: 3 core areas affected
socail interactions
communication
behaviour
ASD: presentation
Usually presents before age of 3 years old and deficits are found in 3 key areas
1) Social Interaction
* Lack of eye contact
* Delay in smiling
* Avoids physical contact
* Unable to read non-verbal cues
* Difficulty establishing friendships
* Not displaying a desire to share attention (i.e. not playing with others)
2) Communication
* Delay, absence or regression in language development
* Lack of appropriate non-verbal communication such as smiling, eye contact, responding to others and sharing interest
* Difficulty with imaginative or imitative behaviour
* Repetitive use of words or phrases
3) Behaviour
* Greater interest in objects, numbers or patterns than people
* Stereotypical repetitive movements. There may be self-stimulating movements that are used to comfort themselves, such as hand-flapping or rocking.
* Intensive and deep interests that are persistent and rigid
* Repetitive behaviour and fixed routines
* Anxiety and distress with experiences outside their normal routine
* Extremely restricted food preferences
ASD: investigations
- specialist doctor.
- involves taking a detailed history of child devlopment, behaviour and communication
- involves talking to nursery, school
- speech and language review
ASD: management
Management
Cannot be cured. Management also depends on severity of the child condition. MDT and psychosocial approach
* Child psychology and child and adolescent psychiatry (CAMHS)
* Speech and language specialists
* Dietician
* Paediatrician
* Social workers
* Specially trained educators and special school environments
* Charities such as the national autistic society
risk factors of ASD
- Older parents
- Prematurity
- Low birth weight
- Birth injury or trauma
- Birth defects
- Meconium aspiration syndrome—when the baby inhales stool from the fluid in the womb
- Anemia—a low level of healthy red blood cells
- Blood type incompatibility between the mother and baby
- The risk of having a child with ASD is also higher in mothers who took antidepressants during pregnancy.
- Genetic problems, such as Fragile X syndrome, Rett syndrome, Down syndrome, or tuberous sclerosis
- Epilepsy
ADHD risk factors
- Genetics—People who have a parent or sibling with ADHD are more likely to get it themselves. Twins are also more likely to both have ADHD.
- Birth factors—Being born very early or having a very low birth weight
- Factors in the mother during pregnancy, such as:
- Smoking
- Using drugs or drinking alcohol
- Using certain medicines, such as corticosteroids and antidepressants
- Mental health problems
- High blood pressure
- Hyperthyroidism
- Exposure to certain environmental toxins, such as lead
- Toxins—Exposure to toxins like lead raises the risk of ADHD in children.
Eating disorders: background
An unhealthy and distorted obsession with body image and food
ED: risk factors
- Female
- Personality disorder
- OCD
- Anxiety
- Genetic component likely
- low self esteem
- childhood trauma e.g. sexual abuse
Anorexia nervosa presentation
- Patient feels overweight despite evidence of normal or low body weight
- Involves obsessively restricting calorie intake with the intention of losing weight
- Patient may exercise excessively and may use diet pills or laxatives to restrict absorption of food
- Key features
o Excessive weight loss
o Amenorrhoea
o Lanugo hair is fine, soft hair across most of the body
o Hypokalaemia
o Hypotension
o Hypothermia
o Changes in mood, anxiety and depression
o Solitude
complications of AN
- Cardiac complications:
- Arrhythmia
- Atrophy
- Sudden cardiac death
complications of AN
- Cardiac complications:
- Arrhythmia
- Atrophy
- Sudden cardiac death
Bulimia nervosa presentation
- Normal body weight
- Weight fluctuates
- Involves binge earing followed by “purging”
o Inducing vomiting or taking laxatives - Key features
o Alkalosis (vomiting HCL)
o Hypokalaemia
o Erosion of teeth
o Swollen salivary glands
o Mouth ulcers
o GORD
o Russels sign- calluses on knuckles
Binge eating presentation
Binge eating disorder is characterised by episodes where the person excessively overeats, often as an expression of underlying psychological distress. This is not a restrictive condition like anorexia or bulimia, and patients are likely to be overweight.
Binges may involve:
* A planned binge involving “binge foods”
* Eating very quickly
* Unrelated to whether they are hungry or not
* Becoming uncomfortably full
* Eating in a “dazed state”
management of ED
Management
- Self help resources
- Counselling
- Cognitive behavioural therapy (CBT)
- Addressing other areas of life, such as relationships and past experiences
- SSRIs (fluoxetine– can be used due to their ability to help people put on weight
Severe cases may require admission for observed refeeding and monitoring for refeeding syndrome.
refeeding syndrome: background
Occurs when people who are severely malnourished begin eating again.
refeeding syndrome pathophysiology
Metabolism in the cells and organs dramatically slows during prolonged periods of malnutrition. As the starved cells start to process glucose, protein and fats again they use up magnesium, potassium and phosphorus. This leads to:
- Hypomagnesaemia
- Hypokalaemia
- Hypophosphataemia
who is high risk of refeeding syndrome
High risk
- BMI <20 and had little to eat for 5 days
- 15% weight loss (unintentional) in last 3-6 months
- Electrolyte levels e.g. K, Phos, Mg (if low)
- Alcohol abuse, use of insulin, chemotherapy, antacids, diuretics
- Malabsorption e.g. chronic vomiting, diarrhoea
complications of refeeding syndrome
Complications
- Cardiac arrhythmias
- Heart failure
- Fluid overload
management of refeeding syndrome
- Starting nutrition support at a maximum of 10kcal/kg/day, increasing levels slowly to meet or exceed full needs by 4-7 day
- Magnesium, potassium, phosphate and glucose monitoring along with other routine bloods
- Fluid balance monitoring
- ECG monitoring may be required in severe cases
- Supplementation with electrolytes and vitamins, particularly B vitamins and thiamine
down syndrome: background
- A genetic disorder caused by the presence of all or part of a third copy of chromosome 21
- Gives characteristic dysmorphic features
- Associated with a number of conditions
- Severity varies between individuals
DS: pathophysiology
- Trisomy 21- chromosome 21
DS: RF
- Older mothers >35
DS: investigations
Antenatal screening
Antental testing
genetic testing
DS: Antenatal screening
- combined test
- triple test
- quadruple test
combined test
11-14 weeks
1) US – nuchal translucency
2) Blood tests
- Beta-HCG (higher=higher risk)
- PAPPA (lower=lower)
triple test
14 and 20 weeks
Blood test
- Beta-HCG (higher=higher)
- AFP (lower= higher risk)
- Serum oestriol (lower= higher risk)
quadruple test
14 and 20 weeks
* Identical to triple + maternal inhibin -A
DS: antenatal tests
o Chorionic villus sampling
o Amniocentesis
o Non-invasive prenatal testing (NIPT)- simple blood test from mother
presentation of DS
Dysmorphic Features
- Hypotonia (reduced muscle tone)
- Brachycephaly (small head with a flat back)
- Short neck
- Short stature
- Flattened face and nose
- Prominent epicanthic folds
- Upward sloping palpebral fissures
- Single palmar crease
complications of DS
- Learning disability
- Recurrent otitis media
- Deafness. Eustachian tube abnormalities lead to glue ear and conductive hearing loss.
- Visual problems such myopia, strabismus and cataracts
- Hypothyroidism occurs in 10 – 20%
- Cardiac defects affect 1 in 3, particularly ASD, VSD, patent ductus arteriosus and tetralogy of Fallot
- Atlantoaxial instability
- Leukaemia is more common in children with Down’s
- Dementia is more common in adults with Down’s
management of DS
Management
- Occupational therapy
- Speech and language therapy
- Physiotherapy
- Dietician
- Paediatrician
- GP
- Health visitors
- Cardiologist for congenital heart disease
- ENT specialist for ear problems
- Audiologist for hearing aids
- Optician for glasses
- Social services for social care and benefits
- Additional support with educational needs
- Charities such as the Down’s Syndrome Association
management of DS
Management
* Occupational therapy
* Speech and language therapy
* Physiotherapy
* Dietician
* Paediatrician
* GP
* Health visitors
* Cardiologist for congenital heart disease
* ENT specialist for ear problems
* Audiologist for hearing aids
* Optician for glasses
* Social services for social care and benefits
* Additional support with educational needs
* Charities such as the Down’s Syndrome Association
DS check ups
- Regular thyroid checks (2 yearly)
- Echocardiogram to diagnose cardiac defects
- Regular audiometry for hearing impairment
- Regular eye checks
DS Prognosis
Prognosis varies depending on the severity of the associate complications. The average life expectancy is 60 years.
cerebral palsy background
- Permanent neurological problems resulting from damage to the brain around the time of birth
- Not progressive , however nature of symptoms may change over time during growth and development
- Huge variation in severity and type of symptoms
pathophysiology of CP
damage to the brain around time of birth
Antenatal:
- Maternal infections
- Trauma during pregnancy
Perinatal:
- Birth asphyxia
- Pre-term birth
Postnatal:
- Meningitis
- Severe neonatal jaundice
- Head injury
pathophysiology of CP
UPPER MOTOR NEURONE DISORDER- damage to the brain around time of birth
Antenatal:
- Maternal infections
- Trauma during pregnancy
Perinatal:
- Birth asphyxia
- Pre-term birth
Postnatal:
- Meningitis
- Severe neonatal jaundice
- Head injury
risk factors for CP
- Hypoxic-ischaemic encephalopathy
- Low birth weight
- Premature birth
- Multiple births e.g. twins
- Infertility treatments
- Infections such as chickenpox, rubella, cytomegalovirus
- Birth complications e.g. detachment of placenta, uterine rupture, umbilical cord problems
CP presentation
Presentation
Becomes more evident during development
- 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
CP management
MDT approach
- Physiotherapy to stretch and strengthen muscles and prevent contractures
- Occupational therapy
- SALT
o May require NG tube or PEG if swallow affected - Dietician
- Orthopaedic surgeons- to release contractures or lengthen tendons
- Paediatricians
o Muscle relaxants e.g. baclofen
o Anti-epileptic drugs for seixures
o Glycopyrronium bromide for drooling - Social workers for benefits and support
- Charities
types of cerebral palys
- Spastic: hypertonia (increased tone) and reduced function resulting from damage to upper motor neurones
- Dyskinetic: problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems. This is the result of damage to the basal ganglia.
- Ataxic: problems with coordinated movement resulting from damage to the cerebellum
- Mixed: a mix of spastic, dyskinetic and/or ataxic features
Spastic CP is also known as pyramidal CP. Dyskinetic CP is also known as athetoid CP and extrapyramidal CP.
monoplegia
one limb affected
hemiplegia
one side affected
diplegia
four limbs affected, mostly legs
quadriplegia
four limbs are affected more severely, often with seizures, speech disturbance and other impairments
CP Complications
- Learning disability
- Epilepsy
- Kyphoscoliosis
- Muscle contractures
- Hearing and visual impairment
- Gastro-oesophageal reflux
Neurological examination for CP
You can gain a lot of information about a child from their gait:
Scissor walking
- Hemiplegic / diplegic gait: indicates an upper motor neurone lesion
- Broad based gait / ataxic gait: indicates a cerebellar lesion
- High stepping gait: indicates foot drop or a lower motor neurone lesion
- Waddling gait: indicates pelvic muscle weakness due to myopathy
- Antalgic gait (limp): indicates localised pain
Hemiplegic and diplegic gait most common in CP
- Increased muscle tone and spasticity in legs
- Legs will be extended with plantar flexion of feet and toes
upper motor neurone vs LMN
CP is UMN
o Good muscle bulk
o Increased tone
o Brisk reflexes
o Slightly reduced power
