Child, learning disability + old age psychiatry Flashcards

1
Q

Autism spectrum disorders

A

Developmental disorder, triad of impaired social interaction + communication difficulties + stereotyped behaviours/interests

Develops before age 3

M>F, genetics/FH linked, more in premature babies

Common features:

  • Social: few social gestures, poor eye contact, late social smile/response to name/interest in others, low awareness of social rules, difficulty with sustaining relationships
  • Behavioural: restricted, repetitive stereotyped behaviour e.g. rocking, upset at change in routine, prefer the same food/clothes/games, fascination with sensory aspects of environment
  • Communication: delayed speech, echolalia (repetition of words)
  • Asperger’s: not really a thing anymore (?see paeds). Like ASD but doesn’t cause impairment in language

Management:

  • bio: treat other disorders e.g. ADHD, melatonin for sleep disorders if severe, antipsychotics sometimes used for severe behaviour
  • psych: CBT if can engage, psychoeducation for families
  • social: modify environmental factors, support with daily living skills/coping strategies, special schooling
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2
Q

ADHD (hyperkinetic disorder)

A

More severe than individuals at same stage of development, present in more than 1 situation (eg home and score):

  • Inattention e.g. not listening when spoken to, distractible, forgetting belongings
  • Hyperactivity: restless, fidgeting, excessive talking, difficulty doing quiet activities
  • Impulsivity: difficulty waiting turn, interrupting others, temper tantrums

Common to also have ASD/dyslexia/mood disorders

Always check hearing!

M:

  • drugs if severe - methylphenidate, atomoxetine or dexamfetamine. drug holiday in school holidays
  • psychoeducation, CBT, behavioural training (reinforce positive behaviour, manage disruptions)
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3
Q

Conduct disorder

A

Repetitive severe pattern of antisocial behaviour - aggression, destruction of property, deceitfulness, major violations of social expectations e.g. stealing/violence to animals etc

RF: male, child abuse, poor SES, parental psychiatric disorders, family conflict, rejection, inconsistent parenting

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4
Q

Emotional disorders of childhood/adolescence

A
  • GAD: free-floating anxiety, fears of death/loss, somatic manifestations (nausea, abdo pain, headaches, sweating, palpitations), panic attacks (sudden onset, extreme fear, faintness, physical sx)
  • Separation anxiety disorder: somatic sx, nightmares, school refusal
  • OCD: obsessional thoughts + compulsive actions related to these
  • Phobic disorders
  • PTSD: persistently re-experiencing trauma, avoiding associated stimuli, increased arousal (sleep disturbance, irritability, poor concentration)
  • Depression: persistent low mood, anhedonia, not always biological sx. M: CBT, fluoxetine has to be initiated by a specialist
  • Eating disorders: rare in pre-adolescents, similar sx to adults, may cause delays in puberty + growth
  • Psychotic illness - rare pre-puberty
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5
Q

What is dementia?

A

Generalised decline of memory, intellect + personality, without impairment of consciousness, leading to functional impairment of ADLs

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6
Q

What may cause dementia?

A

Irreversible:

  • Neurodegenerative: AD, FTD, DLB, Parkinson’s disease dementia, Huntington’s disease
  • Vascular: VD, multi-infarct dementia, post-stroke
  • Traumatic head injury
  • Infections: HIV, encephalitis, syphilis, CJD
  • Toxins: alcohol, BZD, barbiturates

Reversible:

  • Normal pressure hydrocephalus (dementia, urinary incontinence + gait disturbance)
  • Brain tumours
  • Chronic subdural haematoma
  • Vitamin deficiencies: B12, folic acid, thiamine, nicotinic acid
  • Endocrine: Cushing’s syndrome, hypothyroidism
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7
Q

Alzheimer’s dementia

A

Degeneration of cholinergic neurones causing ACh deficiency. A/w neurofibrillary tangles, beta-amyloid plaques, cortical atrophy (often hippocampal), widened sulci, enlarged ventricles

Most common type. Early onset <65y likely familial, late onset more common, insidious onset

Loss of memory (short term then long term), disorientation to T+P, impaired executive function (problem solving, abstract thinking, judgement, planning), visuospatial problems (getting lost, driving issues), language disturbances (finding words, vocab etc), apraxia (inability to carry out previously learned purposeful movements), agnosia (impaired recognition of sensory stimuli e.g. auditory agnosia), non-cognitive sx (perception-hallucinations, thought content-delusions, emotion-depresion/apathy, behaviour-wandering/aggression/restlessness)

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8
Q

Vascular dementia

A

Stroke/multiple infarcts/chronic arteriosclerosis.

  • abrupt/gradual onset, stepwise deterioration
  • personality changes + emotional depression/apathy occur earlier than memory loss. confusion. neurological signs (often UMN). signs of CV disease
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9
Q

Dementia with Lewy Bodies

A

If have PD and develop dementia after 12m then have PD + dementia; as opposed to DLB where dementia + parkinsonian features begin within 12m of each other

Lewy body protein in brainstem neurones/substantia nigra - within brainstem cause dopaminergic loss and parkinsonian sx, outside brainstem cause cholinergic loss

CF: day to day fluctuations in cognitive performance, recurrent visual hallucinations, motor signs of parkinsonism (tremor, rigidity, bradykinesia), recurrent falls/syncope , severe sensitivity to antipsychotic drugs

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10
Q

Fronto-temporal dementia

A

Atrophy of frontal + temporal lobes, subtype is Pick’s disease which involves Pick bodies

insidious development 50-60y, FH in 50%.

Early personality changes (disinhibition, apathy, restlessness), worsening social behaviour, repetitive behaviour, language problems. Insight lost early, memory preserved in early stages

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11
Q

Alcoholic dementia

A

Age-disproportionate cortical + white matter atrophy

Often gradual onset. Cognitive status fluctuates with drinking/withdrawal episodes

Memory problems, frontal features, depression common

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12
Q

Investigations in suspected dementia?

A
FBC-infection, anaemia
U+E
Calcium
LFTs
Glucose-hypos
Vit B12+folate
TFTs-hypothyroidism

Sometimes may do imaging - esp if <60/sudden decline/focal CNS signs - to r/o tumours abscesses + SDH.

Other specialist tests may be done for less common types but AD is a clinical diagnosis

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13
Q

Management of dementia

A
  • Inform DVLA
  • Advance planning
  • Optimise CV RF
  • Social support groups, assistance with ADLs, community dementia teams, home nursing, meals on wheels, befriending, massage, pet therapy
  • Pharmacological:
  • AChE inhibitors (donepezil, galantamine, rivastigmine). Mild-mod AD/DLB for non-cognitive sx that cause distress. Cautioned in arrhythmia + COPD + PUD, galantamine CI in severe hepatic/renal impairment. S/e: GI upset, bradycardia, muscle spasms. Rivastigmine can cause EPSEs
  • Memantine: NMDA receptor antagonist. Moderate AD/if AChE inhibitors CI. Useful for behavioural sx
  • Avoid: anticholinergics (cognitive deterioration), BZDs (falls, cognitive decline), antipsychotics (due to risk of stroke/falls/cognitive decline, may need acutely as a last line)
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14
Q

Causes of delirium

A

Acute transient global organic disorder of CNS function causing impaired consciousness + attention

‘He is not maad’

  • Hypoxia (resp failure, MI, HF, PE)
  • Endocrine (high/low thyroid, high/low glucose, Cushing’s)
  • Infection (UTI, pneumonia, encephalitis, meningitis)
  • Stroke/other brain stuff like RICP/SOL/trauma/epilepsy
  • Nutritional (low thiamine, nicotinic acid, B12)
  • Other (severe pain, sensory deprivation, sleep deprivation, relocation)
  • Theatre (post-op period due to anaesthetic/opiates)
  • Metabolic (hypoxia, electrolyte imbalance, hypoglycaemia, hepatic or renal impairment)
  • Abdominal (faecal impaction, malnutrition, urinary retention)
  • Alcohol (intoxication, withdrawal)
  • Drugs (BZD, opioids, anticholinergics, anti-Parkinsonian, steroids)
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15
Q

Features of delirium

A

Acute onset, fluctuating course, often worse at night

Features of delirium:

  • Disordered thinking
  • Emotions: euphoric/fearful/depressed/angry
  • Language impairment
  • Illusions
  • Reversal of sleep-wake pattern
  • Inattention
  • Unaware/disoriented
  • Memory deficits

Types:

  • Hypoactive: lethargy, reduced motor activity, apathy
  • Hyperactive: agitation, irritability, restlessness, delusions, hallucinations
  • Mixed
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16
Q

Management of delirium

A

Look for the cause:

  • Bloods - FBC, U+E, LFT, calcium, glucose, CRP, TFTs, B12/folate/ferritin (haematinics)
  • Urinalysis
  • ECG
  • May do further infection screening like cultures, CXR. May do ABG, CT head

Do AMT etc

Actual management:

  • treat the cause!
  • reassure pt. re-orientation to TPP
  • appropriate environment: quiet well-lot room, consistency in staff, encourage friends/family, optimise sensory acuity (clock, glasses)
  • for behaviour: encourage oral intake, fluid balance chart, verbal + non-verbal de-escalation techniques. may need oral low dose haloperidol or olanzapine, avoid BZDs unless delirium is due to alcohol withdrawal
17
Q

What are learning disabilities?

A

Incomplete development of the mind causing a wide range of functional impairment

Majority are mild but can be severe

18
Q

Causes of learning disabilities

A
  • genetic - Down’s syndrome, fragile X, cri du chat, prader-willi, neurofibromatosis, homocystinuria, galactosaemia, PKU, T18, T13, etc etc etc
  • antenatal: congenital infection, malnutrition, intoxication, endocrine e.g. hypothyroidism, physical injury/hypoxia, APH, pre-eclampsia
  • perinatal: birth asphyxia, IVH, neonatal sepsis, prematurity, neonatal hypoglycaemia/sepsis/meningitis/kernicterus
  • environmental: neglect, NAI, malnutrition
19
Q

Common co-morbidities in patients with learning disabilities

A

Physical

  • primary: spasticity, hypothyroidism, cerebral palsy, impaired hearing/vision, epilepsy (much more common than in general population + more treatment-resistant)
  • secondary: incontinence, constipation, fractures, obesity, GORD, dental caries, infection

Psychiatric:

  • ASD (up to 1/3), ADHD
  • anxiety + depressive disorders, schizophrenia, personality disorders
  • eating disorders
  • early-onset Alzheimer’s
  • -> presentation different as may be limited communication/diagnostic shadowing.
  • ->increased vulnerability + adverse life experiences
  • ->atypical presentations e.g. change of behaviour, loss of skills e.g. incontinence, not doing things they used to enjoy, sleep + weight changes
20
Q

Congenital syndromes a/w learning disabilities

A
  • Down’s syndrome: T21. LD, good natured sociable phenotype, more early onset dementia, depression, ASD/OCD.., medical problems, physical dysmorphic facies, structural abnormalities e.g. ASD/VSD/ToF
  • Fragile X: MV prolapse, large protruding ears, long face, high arched palate, flat feet, soft skin, lax joints
  • Prader-Willi: hypotonia + developmental delay, obesity, hypogonadism, behavioural problems
  • Cri du chat: high pitched cry, low birth weight, feeding difficulties
21
Q

Physical features of Trisomy 21

A

upslanting palpebral fissure, round face, occipital & nasal flattening, brushfield spots on iris, brachycephaly, low-set small ears, epicanthic folds, open mouth/protruding tongue, strabismus (squint), sandal gap deformity, single palmar crease, big toes widely spaced

22
Q

Medical problems a/w trisomy 21

A

heart (ASD, VSD, ToF), hearing loss, visual disturbance (cataracts, strabismus, keratoconus), GI problems (oesophageal/duodenal atresia, Hirschsprung’s, coeliac, enlarged colon, umbilical hernia), hypothyroidism, haematological malignancies (AML, ALL), increased incidence of AD, epilepsy (infantile spasms, tonic clonic seizure in middle age), obesity, C-spine abnormalities, recurrent respiratory tract/ear infections, OSA