Elective Preparation Flashcards

1
Q

What are the core clinical characteristics of ASD?

A

Impairments in two areas of functioning (social communication and social interaction), as well as restricted, repetitive patterns of behaviour, interests or activities. Must be present from early childhood.

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2
Q

Where is ASD found in the DSM-5?

A

Under neurodevelopmental disorders

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3
Q

How do we determine ASD severity?

A

Three levels:

1: requires support
2: requires substantial support
3: requires very substantial support

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4
Q

How prevalent is ASD?

A

1% in the UK

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5
Q

Give three red flags of ASD in the second year of life.

A
Lack of showing
Lack of coordination of nonverbal communication
Lack of sharing interest or enjoyment
Repetitive movements with objects
Lack of appropriate gaze
Lack of response to name
lack of warm, joyful expressions
Unusual prosody
Repetitive movements or posturing of body
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6
Q

Should we screen for ASD?

A

There are screening tools with up to 70% specifities and sensitivities, however only if there’s a suitable treatment and the means to provide this treatment. Examples include the modified checklist for autism in toddlers (M-CHAT) and the childhood autism spectrum disorders test (CAST)

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7
Q

What was autism thought to be due to in the 1950s/60s?

A

The defective upbringing of children by cold and rejecting parents, thereby leaving the child with no alternative but to seek comfort in solitude

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8
Q

Give five risk factors for ASD

A
  • Siblings with autism
  • Being a twin (especially monozygotic)
  • Valproate use during pregnancy
  • Folic acid use reduces risk
  • Epigenetics
  • Parental history of schizophrenia-like psychosis
  • Parental history of affective disorder
  • Parental history of another mental or behavioural disorder
  • P/Maternal age of over 40y
  • Low birth weight
  • Prematurity
  • Presence of birth defects
  • Male gender
  • Threatened abortion at less than 20 weeks
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9
Q

How would a child with ASD react to a windup toy?

A

A typical child at 12m shifts his eye gaze from the windup toy to the clinician and then coordinates his eye gaze with smiling. A child with ASD becomes hyper-focused on the windup you and doesn’t look at or engage with adults.

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10
Q

What is stimulus overselectivity?

A

Children with ASD exhibit overly selective attention to some particular stimuli, not to the gestalt of what is being seen or heard (like making a puzzle not using the image to be built but paying attention only to the shape of the pieces). Also seen with intellectual disabilities.

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11
Q

Give examples of peer relation behaviours seen in ASD.

A
  • Not looking into the eyes of approaching adults
  • Failing to orient towards biological motion
  • Using nonverbal behaviours less often than typically developing children (eye contact, gestures, body postures, facial expressions)
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12
Q

How can we quantify impairments in communication?

A
  • Delay in, or total lack of development of spoken language, no accompanied by compensatory attempts
  • Marked impairment in the ability to initiate or sustain conversations
  • Stereotyped, repetitive or idiosyncratic language
  • Lack of varied, spontaneous imitative or make-believe play
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13
Q

How might a child with ASD react to a popping balloon?

A

Over-reactive to sensory input, covers ears in anticipation of it making a loud noise, reach to mother for comfort

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14
Q

Name two disorders ASD is associated with.

A

Fragile X syndrome

Rett’s disorder

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15
Q

What are the differential diagnoses of ASD

A
  • Severe psychosocial deprivation
  • Intellectual disability
  • Rett’s disorder
  • Receptive-espressive language disorders
  • Separation anxiety
  • Childhood schizophrenia
  • ADHD
  • OCD
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16
Q

How do we treat ASD?

A
  • Education, with special attention to social, communication, academic and behavioural development
  • Accessible community support
  • Psychological and medical treatments
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17
Q

How do we treat ASD pharmacologically?

A

Medication is justified only to treat co-morbid conditions e.g. ADHD, not for the core symptoms of ASD, and in the management of challenging behaviours e.g. aggression and self-harm that do not response to other approaches. There is good evidence that risperidone can be helpful for the latter.

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18
Q

What was the former name of ADHD and why was its name changed?

A

Used to be called minimal brain damage. Then changed to minimal brain dysfunction when realised not all children had brain lesions. Then changed to hyperkinetic disease characterised by restlessness and distractibility. Then changed to ADHD when the role of inattention was recognised.

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19
Q

What was the first effective treatment for ADHD?

A

Benzedrine, which could decrease hyperactivity and improve attention and academic performance.

20
Q

What is the worldwide prevalence of ADHD?

A

Between 5-7%

21
Q

Describe the aetiology of ADHD.

A

Familial disorder, with likely gene-environment interactions. First degree relatives show a five- to ten-fold increased risk of developing the disorder themselves, and likely epigenetic link.

22
Q

Give four environmental RFs for ADHD

A

Pre/perinatal factors: low birth weight, prematurity, in-utero exposure to maternal stress, maternal obesity, HTN, cigarrette smoking, alcohol, acetaminophen or valproate use, illicit substance use

Environmental toxins: leads, organophosphate pesticides
Nutritional deficiencies: zinc, magnesium, iron, omega-3 polyunsaturated fatty acids
Nutritional surpluses: sugar, artificial food colorings, low/high IgG foods
Psychosocial factors: low income, family adversity, harsh or hostile parenting

23
Q

Which are the main two neurotransmitters than have been studied in ADHD pathophysiology?

A

Dopaminergic and noradrenergic.

Methylphenidate and amphetamines target the sodium-dependent noradrenaline transporter

Atomoxetine targets the sodium-dependent noradrenaline transporter

24
Q

How does an ADHD brain model differently to a typical childs?

A

The ADHD brain matures more slowly than the brain from typically developing children.

25
Q

Give manifestations of inattention.

A

Mind wandering whilst performing a task
Difficulty sustaining attention in tasks or activities
Disorganization
Struggling to listen when spoken to
Struggling to accomplish and to finish tasks activities
Avoidance of tasks that need more mental effort
Misplacing objects needed to perform tasks or activities
Distractibility by external stimuli
Forgetfulness about daily activities

26
Q

Give presentations of hyperactivity.

A

Excessive motor activity when inappropriate
Fidgeting
Tapping
Inappropriate talkativeness
Often on the go, “driven by a motor”
Blurting out answers before a question has been finished
Interrupting others or intruding

27
Q

What is impulsivity?

A

Making decisions or performing actions without planning

28
Q

What are the three ADHD presentations?

A

Predominantly inattentive
Predominantly hyperactive/impulsive
Combined

29
Q

What is the difficulty with diagnosing ADHD in preschoolers?

A

A degree of impulsivity and hyperactivity is developmentally appropriate

30
Q

What are the most common co-morbidities seen with ADHD?

A

Oppositional defiant disorder (ODD), conduct disorder (CD), intellectual disability, learning disorders, language disorders, sleep disorders, enuresis, developmental motor coordination disorders, depressive and anxiety disorders, tic disorders, autism spectrum disorders

31
Q

How is ADHD diagnosed?

A

6/9 symptoms of inattention
OR
6/9 symptoms of hyperactivity/impulsivity

Symptom onset before 12
For at least 6 months
Present in two or more settings (school, work, home)
Causing significant impairment

32
Q

How does relative immaturity impact ADHD diagnosis?

A

Children in the same grade at school are a
heterogeneous group with some, born earlier, being older than others, born later.
Age difference can be as large as 12 months, representing up to 15% of their young
lives. Studies have shown that children who are younger than their classmates
are more likely to be diagnosed with ADHD (Caye et al, 2019a). Although the
reasons for this are not clear, it could be due to younger (less mature) children
being incorrectly diagnosed as having ADHD (false positives), or younger children
with ADHD in the same school grade having a more severe clinical presentation,
making easier its recognition. Irrespective of the reason, this issue should be taken
into consideration not just by clinicians but also by teachers.

33
Q

Give three potential negative outcomes of ADHD

A

Worse QoL
Higher suicide rates
Higher risk of parental separation

34
Q

How do we treat ADHD?

A

Psychoeducation
Behavioural and psychosocial treatment e.g. behaviour classroom interventions, social and organisational skills training, meditation-based therapy and cognitive therapy
Stimulants
Non-stimulants (the noradrenaline reuptake inhibitor atomoxetine and the ɑ2-adrenergic agonists clonidine and guanfacine)

35
Q

What is the limitation of using methylphenidate?

A

Short half-life, thus requiring two or three doses during the day for optimal benefit

36
Q

How does concerta work to slow down absorption?

A

Osmotic pump mechanism with 22% of the dose available as immediate release

37
Q

Why are amphetamines less often used?

A

Concerns about potential for abuse
Not commercially available in some countries
Vyvanse (lisdexamfetamine) is the first line amphetamine

38
Q

How do stimulants act?

A

Impact on dopamine and/or noradrenaline pathways, which support attention, reward processing and activity

39
Q

Give five SEs of adhd medication use

A
Loss of appetite
Growth retardation
Insomnia
Hepatotoxicity (atomoxetine)
Abnormal BP or cardiac function
Tics
Anxiety
Drug misuse - ? diversion (selling on)
40
Q

Where can medication holidays be useful when treating ADHD?

A

If symptoms are pronounced mostly at school or if medication causes significantly decreased appetite or insomnia

41
Q

What is enuresis?

A

Involuntary (or intentional) nocturnal wetting in children 5 years of age or older after organic causes have been ruled out. It must have persisted for at least three months to be considered a disorder.

42
Q

What is the difference between primary and secondary enuresis? Why is it important?

A

Primary is if child has been dry for less than 6 months
Secondary is if there’s a relapse after a dry period of at least 6 months

Children with secondary have experienced stressful life-events (e.g. separation of parents, birth of siblings) more often and have higher rates of co-morbid psychiatric disorders.

43
Q

How many times should children go to the toilet every day?

A

5-7

44
Q

What causes dysfunctional voiding?

A

A disorder of the emptying phase: instead of relaxing the sphincter muscle, it is contracted paradoxically. Straining and an interrupted urine stream are indicative of this disorder.

45
Q

What is the most common comorbid disorder in enuresis?

A

ADHD, in up to 10%

46
Q

How can we treat enuresis?

A

Alarm treatment. It contains a sensor that, when becomes wet, goes off and wakes up the child.

47
Q

What is the use of desmopressin?

A

Antienuretic, it is a synthetic analogue of ADH, however after discontinuing most children relapse.