A-C Flashcards

(47 cards)

1
Q

What is ADHD?

A

Disorder characterized by attention deficit, hyperactivity and impulsiveness for >6m and causing impairment in more than one setting.

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2
Q

What is the aetiology of ADHD?

A

Genetic factors: twin concordance. Environmental factors: intrauterine complications, maternal smoking and alcohol use. Related to other behavioral disorders.

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3
Q

What is the epidemiology of ADHD?

A

9% school age children affected.

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4
Q

What would you find in the history/ exam of ADHD?

A

Attention deficit: inability to sustain mental effort, to concentrate on one thing

Hyperactivity: running around incessantly, loudness, talking

Impulsiveness: can not wait in line or take turns, talk over others, change subject

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5
Q

What would you find in the investigations of ADHD?

A

Full developmental, pregnancy, family, social and educational history.

Conners rating questionnaire of Strengths and Difficulties. Exclude medical conditions (seizures, visual or hearing loss, hypothyroidism). ECG required and full cardio FHx before starting stimulants.

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6
Q

What is the management of ADHD?

A

Child health education, community outreach for family and child. Individual child therapy for behavior modification and CBT. Parent training programs.

Drug therapy:

· Methylphanidate/Dexamphetamine (>6yo): CNS stimulant. SE include insomnia, loss of appetite, weight loss, nervousness, headache, palpitations and tachycardia. Height, weight, BP monitoring 6monthly.

· Atomoxetine (>6y): Selective NA reuptake inhibitor, second line. SE abdominal pain, vomiting, ow appetite, liver damage, irritability and mood swings, suicidal intentions.

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7
Q

What are the complications and prognosis of ADHD?

A

Negatively affects education and school performance.

May improve with maturation and age. Children with good input improve into adult life.

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8
Q

What is Autistic spectrum disorder?

A

Developmental disorder affecting social communication, interaction and behavior that are generally stereotypical and repetitive and lacking imagination. Umbrella that ranges between low and high functioning.

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9
Q

What is the aetiology of Autistic spectrum disorder?

A

Genetic factors: 80% concordance between twins. RF maternal rubella infection, high paternal age. NO LINK WITH MMR!

Related with TS, Fragile X, Epilepsy

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10
Q

What is the epidemiology Autistic spectrum disorder? of

A

NAS prevalence UK 535k. Increasing in prevalence.

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11
Q

What would you find in the history/ exam of Autistic spectrum disorder?

A

Motor: stereotypical repetitive movements, mannerisms. Uncoordinated.

Behavioral: ritualistic behaviors, disruption of which leads to violent outbursts. Interests and obsessions.

Social: indifference to others, avoiding eye contact, preferring to be alone, lack of understanding of social cues and sharing.

Speech: delayed speech and inability to express wants and needs, echolalia, socially inappropriate comments.

LD: varies with spectrum. May have sensory /sleep abnormalities/eating/toilet.

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12
Q

What would you find in the investigations of Autistic spectrum disorder?

A

Strengths and Difficulties questionnaire for parent and teacher. Assessment in class.

Bloods: for fragile X, FBC, ferritin, TFT, Lead.

Developmental assessment EEG, seizure observation.

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13
Q

What is the management of Autistic spectrum disorder?

A

MDT approach: initiated ASAP. SALT input, OT assessment, parental and child education on toileting school behavior rewarding etc. SPELL and TEACCH approaches. Parental support via charities and support groups.

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14
Q

What are the complications and prognosis of Autistic spectrum disorder?

A

Poor performance in school, physical abuse by frustrated carers, aggressive and self injurious behavior.

Very varied outcome depending on degree of speech and social impairment, and intellectual ability.

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15
Q

What is Cerebral haemorrage?

A

Bleed in the extradural subdural or subarachnoid space.

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16
Q

What is the aetiology of Cerebral haemorrage?

A

Extradural: direct head trauma causing arterial or venous bleed. Usually trauma on MMA over the pterion.

Subdural: birth trauma, forceps delivery, NAI baby shaking, low BW. Can be chronic (due to tearing of veins between the arachnoid and pia mater) or acute (due to rupture of vein of Galen)

Subarachnoid: AVM and aneurysms. May be due to saccular or Berry aneurysms (haemodynamic stress in arteries in predisposed individuals such as EhDan and Marf)

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17
Q

What is the epidemiology of Cerebral haemorrage?

A

ED mostly under 2y, SD mainly in young infants, SAH rare in children.

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18
Q

What would you find in the history/ exam of Cerebral haemorrage?

A

Symptoms of raised ICP

· Early nausea, vomiting, confusion, drowsiness.

· Later, develop hypertension and bradycardia – Cushing response. Ipsilateral CN3 palsy, papillodema and coma.

EDH: hx of trauma, force and impact, severe headache

aSDH: shock, seizures, coma, retinal haemorrages

cSDH: increasing confusion, headache, sleepiness, macrocephaly, fail to thrive

SAH: tearing pain, sudden onset occipital headache, neck stiff, retinal haemorrage, fever, seizures.

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19
Q

What would you find in the investigations of Cerebral haemorrage?

A

Skull XR: if fracture suspect, especially temporal.

CT head: indicated if there is suspect TBI, best way to detect blood. Indicated if:

· LOC or amnesia>5 min

· GCD<15 if <1, or <14 in >1y

· >3 times vomiting

· Suspected NAI

· PTS but no epilepsy hx

· Suspicion of open or depressed skull fracture or tense fontanelle

· BSF signs: panda eyes, battles sign, CSF leak

· Focal neuro deficit

· Age <1y with bruise, swelling or laceration >5cm on head

· Dangerous mechanism of injury.

LP: Xanthochromia in SAH

Angiography: if ?aneurysm.

20
Q

What is the management of Cerebral haemorrage?

A

C-spine immobilization if fracture is suspect

Secure airway if non patent, vent and blood if required

Immediate high ICP treatment: hyperventilation and hyperosmolar therapy

Extradural/subdural requires surgical evacuation. SAH requires surgical correction.

21
Q

What are the complications and prognosis of Cerebral haemorrage?

A

Hydrocephalus, herniation, vasospasm, hypoxia, rebleeds.

ED: good with immediate management. GCS before surgery corrected with outcome.

cSDH: Depends on cause and on associated brain injury. 3% mortality. 75% normal development at FUp.

aSDH/SAH: over 60% mortality.

22
Q

What is cerebral palsy?

A

Non progressive disorder of movement due to insult to brain parenchyma.

23
Q

What is the aetiology of cerebral palsy?

A

Antenatal 80% - Cerebral dysgenesis or malformation, congenital infection (TRC)

Perinatal 10% - HIE, birth trauma

Postnatal 10% - Meningitis, encephalitis, EDH, IVH, TBI, NAI, high BR (kernicterus), hypoglycaemia.

Assoc w/ epilepsy, LD, development delay, visual impairment, squints,

24
Q

What is the epidemiology of cerebral palsy?

A

2/1k live births.

25
What would you find in the history/ exam of cerebral palsy?
Global developmental delay, poor feeding, tone abnormalities, gait, language difficulties, imapried social skills. Several types. 1. Spastic 70% o Increase tone, brisk reflex, extensor plantar response o Hemiplegia of arm>leg, fisting, abduction of shoulder, flexion of elbow and wrist, pronation of forearm, extension of fingers. à MCA territory damage o Diplegia legs>arms, hypertonic abductors leading to leg scissoring. -> IBH and ventricular damage o Quadriplegia: 4 limbs affected, poor head control, abnormal primitive persistent reflexes. -> Widespread bilateral lesions 2. Dyskinetic 10% o Normal progress up until 9 months, then progressive dystonia accompanied by jerking and writhing involuntary movements. -> abnormal extrapyramidal pathways (BG/Thal) 3. Ataxic 10% o Hypotonia, ataxia of trunk and limbs, postural imbalance and intention tremor. -> Abnormal cerebellar development 4. Mixed 10%
26
What would you find in the investigations of cerebral palsy?
Assess hearing and vision, EEG.
27
What is the management of cerebral palsy?
MDT approach: · Education: school support · Physiotherapy, OT, SALT · May need feeding tube, ortho input · Baclofen and botulinum decrease spasticism and pain · Neurosurgical input may be required to reduce abnormal movements.
28
What are the complications and prognosis of cerebral palsy?
Aspiraiton pneumonia, fail to thrive, scoliosis, hip dislocation. Spastic hemiplegis: delayed then normal gait. Spastic diplegia: characteristic gait with knees flexed and toe walking, adducted hips. Spastic quadriplegia: Poor prognosis due to feeding disability and mobility issues, Die from chest infections form aspirations usually. Dyskinetic: usually can walk independently. Ataxic: most can walk with crutches.
29
What is conduct disorder?
Aggression to people and animals, destruction of property, deceitfulness, theft and violation of rules in more than 12 months. Subdivided into childhood onset and adolescent onset (cutoff 10y).
30
What is the aetiology of conduct disorder?
Environmental risk factor: low SES, homeless, parent drug use, overcrowding, parental mental illness, single parent, large family, child abuse and neglect etc
31
What is the epidemiology of conduct disorder?
CD is the main referral to CAMHS. 4% childhood, 6% adolescent prevalence.
32
What would you find in the history/ exam of conduct disorder?
Childhood: temper tantrums, disobedience, lying, destruction of property, hitting, biting Adolescent onset: vandalism, bullying, shouting, lying, stealing, truancy.
33
What would you find in the investigations of conduct disorder?
CAMHS specialist formal assessment with Child Behavior Checklist CBCL.
34
What is the management of conduct disorder?
Child focused therapy: CBT, behavioral, psychotherapy. Parent training interventions: reward systems, promote daily play, encourage recognition, short specific commands and rewards, calm response to bad behavior. Family interventions with therapist.
35
What are the complications and prognosis of conduct disorder?
Impact on education, comorbid with ADHD, ASD, depression, LD, substance misuse, psychosis. Early conduct disorder are best predictor of future criminality. 50% are diagnosed with antisocial personality disorder and will go on to have substance and alcohol abuse.
36
What are brain tumours can children get?
o Astrocytoma (40%): vary from benign to malignant (GBM) o Medulloblastoma (20%): arise in midline of the posterior fossa, 20% have spinal metastases at diagnosis o Ependymoma (8%): mostly in posterior fossa o Brainstem glioma (8%): poor prognosis o Craniopharyngioma (4%): developmental tumour arising from the squamous remnant of Rathke pouch. Not truly malignant but locally invasive and grows slowly in suprasellar region o Atypical teratoid/rhabdoid tumour
37
How common are brain tumours in kids?
Common, only beaten by leukaemia • In children, almost always primary rather than metastatic • 60% are infratentorial (located below tentorium cerebelli)
38
Which clinical features of brain tumours affect all ages?
o Persistent or recurrent vomiting o Problems with balance, coordination or walking o Behavioural change o Abnormal eye movements o Seizures, without fever o Abnormal head position: wry neck, head tilt or persistent stiff neck
39
Which clinical features of brain tumours affect children and adolescents?
``` o Persistent or recurrent headache o Blurred or double vision o Lethargy o Deteriorating school performance o Delayed or arrested puberty, slow growth ```
40
Which clinical features of brain tumours affect infants?
o Developmental delay o Progressive increase in head circumference, separation of sutures, bulging fontanella o Lethargy
41
Which features are associated with supratentorial tumours?
▪ Seizures ▪ Hemiplegia ▪ Focal neurological signs
42
Which features are associated with midline tumours?
▪ Visual field loss: bitemporal hemianopia | ▪ Pituitary failure: growth failure, diabetes insipidus, weight gain
43
Which features are associated with cerebellar and 4th ventricle tumours?
▪ Truncal ataxia ▪ Coordination difficulties ▪ Abnormal eye movements
44
Which features are associated with brainstem tumours?
▪ Cranial nerve defects ▪ Pyramidal tract signs ▪ Cerebrallar signs: ataxia ▪ Often no raised ICP
45
Which features are associated with spinal tumours?
Spinal tumours can present with back pain, peripheral weakness of arms or legs or bladder/bowel dysfunction
46
What investigations do you do for brain tumours?
• MRI scan • Lumbar puncture may reveal metastases in CSF o Contraindicated in raised ICP
47
What is the management of brain tumours?
``` Surgery o Treat hydrocephalus o Provide tissue diagnosis o Attempt maximal resection • Chemotherapy • Radiotherapy ```