Attention Deficit Hyperactivity Disorder Flashcards

1
Q

Why should childhood disorders be given special consideration?

A
  • Less complex/realistic view of themselves/world.
    • Less self-understanding/no sense of identity.
    • Less past judgements to compare to.
    • No thoughts on future issues.
    • Events become overly important.
    • Highly dependent upon adults.
    • Increased vulnerability.
    • More sensitive to rejection, failure, and disappointment.
    • Problems can become insurmountable, if not “nipped in the bud”.
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2
Q

Why does rapid brain development increase vulnerability to disorder in children?

A
As the brain develops, several processes occur such as:
	Pre-birth: neurulation -> neuronal proliferation -> neural migration
	Lots of different processes occurring at different times, brain maturation occurs into adulthood.
		- Neuronal migration
		- Synapse formation 
		- Synaptic pruning
		- Myelination
		- Connectivity/complexity.
		- Cortical Thinning
	By 1 years old - 70% adult size.
	By 2 years old - 80% adult size.
	Cortex grows by 88% in this time.
	By 5 years old- 90% adult size.
Brain development is highly dependent on environmental factors such as:
	- Stimulation
	- Interaction
	- Responses
	- Experience
	- Diet/growth/environmental factors.
As any of these processes are disrupted or impaired, they can cause a multitude of mental disorders, explaining the high rate.
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3
Q

Outline the criteria for ADHD.

A
  • Attention Deficit
    - Impulsivity
    - Poor concentration
    - Easily distracted.
    • Hyperactivity Disorder
      • Exaggerated motor activity
      • Fidgeting/squirming
      • Aimless running
      • Excessive talking
      • Socially intrusive
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4
Q

What are the functional consequences of ADHD?

A
  • Poor academic achievement- particularly reading
    • Low intelligence
    • Immaturity
    • Low self-esteem
    • Inability to form normal parental relationships
    • Inability to form normal peer/peer relationships
    • Negative views by peers
    • Increased risk of substance abuse
    • Increased risk of anti-social behaviour
    • Abnormality is sometimes subtle- an extension of normal behaviour.
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5
Q

Outline the subtypes of ADHD in DSM-5.

A

Predominantly Inattentive (I)
The majority of symptoms (six or more) are in the inattention category (1) and fewer than six symptoms of hyperactivity-impulsivity are present, although hyperactivity-impulsivity may still be present to some degree. Children with this subtype are less likely to act out or have difficulties getting along with other children. They may sit quietly, but they are not paying attention to what they are doing. Therefore, the child may be overlooked and parents and teachers may not notice symptoms of ADHD.`
Predominantly Hyperactive-Impulsive Type (HI)
Most (six or more) are in the hyperactivity-impulsivity categories (2). Fewer than six symptoms of inattention are present, although inattention may still be present to some degree.
Combined Hyperactive-Impulsive and Inattentive ©
Six or more symptoms of inattention and six or more symptoms of hyperactivity-impulsivity are present.
Most children with ADHD have the combined type.
DSM-5 has a category of OS ADHD- not a full range of criteria.

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6
Q

What differential diagnoses can be made instead of ADHD?

A

GP first port of call- but need child psychiatrist for final diagnosis. Need to discount other causes of hyperactivity/inattention, such as:
- Medical conditions such as hypothyroidism, anaemia, lead poisoning, chronic illness, hearing or vision impairment, substance abuse, medication side effects, sleep impairment, child abuse, (individual differences in behaviour).
- Psychological conditions such as: oppositional conduct disorder, conduct disorder, FAS.
Comorbidities
Many have high levels of anxiety (25%), conduct disorder (10-20%), developmental disorder (10-90%), mood disorder (15-75%), oppositional defiant disorder (35-65%), substance abuse (20-40%), and tics (50%).

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7
Q

Outline and evaluate the psychosocial aetiology of ADHD.

A

Psychosocial (diathesis/stress) biological (IUGR/genetics/neuroanatomical)
IUGR = Intrauterine growth retardation.
Media points fingers at tv viewing, diet (artificial chemicals & sugars) but these do not seem to be factors. Banerjee et al (2007) highlighted psychosocial adversity, pregnancy and delivery complication, maternal smoking, foetal exposure to alcohol, and PCB (polychlorinated biphenyls) as risk factors.

Rutter (1975) six risk factors for neurodevelopmental disorders (not just ADHD), by comparing Isle of Wight children with inner city children:
	1. Severe marital discord
	2. Low social class
	3. Large family size
	4. Paternal criminality
	5. Maternal mental disorder
	6. Foster placement
		\+ maltreatment
		\+ emotional trauma
Symptoms in 10 year old children such as:
-- poor concentration
	- Hypervigilance to perceived fear stimuli
	- Stimulus avoidance
	- Excessive worry
	- Denial
	- Rage
	- Social withdrawal
Factors seem to be
	- Marital distress
	- Family dysfunction
	- Social class
	- Maternal psychopathy
Combination of adversity, not just specific risk-factor. May have a greater risk on outcome rather than onset.
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8
Q

Outline and evaluate the pre/neonatal aetiology of ADHD.

A
  • Children with a history of preterm delivery, also close to term delivery, are at increased risk for clinically verified HKD or ADHD combined type.
    • Children born at term with low birth weights are also at increased risk.
    • Foetal exposure to toxins such as PCBs, lead, mercury.
      • Maternal alcohol: hyperactivity, impulsivity (FAS)
      • Maternal tobacco: 2.7x increase in ADHD, reduces placental function. Link between nicotine and dopamine function. Can affect neuronal proliferation/differentiation. Hypoactivity of dopamine/noradrenaline.
    • Birth complications- pre-eclampsia, hypoxia, prematurity, maternal age/health, duration of labour, etc….
    • IUGR -intrauterine growth retardation
    • All lead to low birth weight (within normal standard deviations)- need to catch up.
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9
Q

Outline and evaluate the genetic aetiology of ADHD.

A
  • High heritability - 75%
    • High MZ concordance
    • Many gene candidate association studies.
    • Genome wide association studies
    • Numerous candidates
    • Genetic candidates
    • Genetic candidates have high biological efficacy.
      • Linked to dopamine function - DS, D5 receptors, DAT: dopamine transporter.
      • Linked to serotonergic function - 5HT1B, SERT: serotonin transporter.
      • Linked to noradrenergic function: NET: noradrenaline transporter.
    • D4 receptor gene strongest candidate.
    • Quite a good idea of genetic contributions to ADHD, consistent pattern of neurotransmitter/synaptic dysfunction.
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10
Q

Outline and evaluate the diathesis-stress model of ADHD.

A

R

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11
Q

Outline and evaluate the biological aetiology of ADHD.

A

R

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12
Q

Outline Methylphenidate (Ritalin) as an ADHD treatment.

A

r

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13
Q

Why is Ritalin potentially useful?

A
  • First line treatment options that has been used since the 1930s.
    • A stimulant (amphetamine derivative)
    • Paradox:
      ○ Stimulant drug enhances activity normally.
      ○ But in ADHD reduces activity/improve cognition?
    • Acts to inhibit DAT function (but not very selective)
      ○ Leads to increase in extracellular dopamine in striatum etc.
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14
Q

What are the problems of using Ritalin to treat ADHD?

A
  • Side effects: decreased appetite, headaches, abdominal discomfort, sleep problems, irritability, motor tics, nausea, fatigue, social withdrawal.
    ○ Increased risk of sudden death, cardiovascular problems, heart attacks.
    • Academic: Short-term gains only.
    • Relationships: Generally improved but not normal.
    • Addiction: Risk of substance abuse- amphetamine compound, but untreated ADHD has greater risk of addiction.
    • Short term gains or long term effectiveness?
      ○ But see MTA (multimodal treatment). 4% had adverse effects in MTA.
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15
Q

Evaluate the extent to which ADHD can be considered to be a dopamine-deficiency disorder.

A

R

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16
Q

Evaluate the involvement of noradrenaline and NET in ADHD.

A

R

17
Q

Outline and evaluate the use of atomoxetine in treating ADHD.

A

R

18
Q

Outline and evaluate non-pharmacological treatments in ADHD.

A

R

19
Q

Evaluate Multimodal Treatment for ADHD

A

R

20
Q

Evaluate the extent to which ADHD can be considered to be a real behaviour.

A

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21
Q

Is Ritalin overused?

A

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22
Q

Why does ritalin increase dopamine and norepinephrine in the prefrontal cortex despite DAT density?

A

ritalin is not necessarily specific to DAT (the dopamine trnasporter) only, it may have affects on the noradrenaline transporter also. atomoxetine (and, as the names usggests SSRIs) are very selective drugs only working on their specific targets: NET (and for SSRIs, the serotonin reuptake transporter (SERT). SO ritalin may also affect other neurotransmitter systems that it comes into contact with. also worth remembering that the drug is not targetted at the striatum, taken as a pill, will (potentiall) be all round the body - and all parts of the brain.