ADHD Flashcards

1
Q

What is the triad of ADHD?

A

Inattention

Hyperactivity Impulsivity.

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2
Q

How is ‘inattention’ defined?

A

Fails to sustain attention, follow through on instructions/work, and listen.

Careless errors

Avoids tasks requiring mental effort

Loses things

Easily distracted.

Forgetting, poor planning.

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3
Q

How is ‘hyperactivity’ defined?

A

Fidgets or squirms

Leaves seat

Excess running about

Unduly noisy

Excess motor activity.

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4
Q

Impulsivity?

A

Blurts answers

Fails to wait in lines

Interrupts others

Excessive talking

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5
Q

What is the comorbidity?

A
  • Conduct disorder
  • Anxiety & Depressive disorder
  • Learning difficulties
  • Tourette’s disorder
  • Soft neuro signs
  • Alcohol and substance misuse
  • Offending
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6
Q

What is the ADHD spiral?

A

ADHD symptoms causes learning difficulties, causing failure at school, leading to low self esteem and isolation.

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7
Q

What are the genetics of family studies?

A

20% of hyper children had parent reporting childhood hyperactivity.

8x increased risk of child ADHD if parent meets ADHD criteria.

BUT- it could still be environmental.

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8
Q

How would you tease out environment vs genes?

A

MZ and DZ twin studies.

MZ twins: If one twin has ADHD, 80% concordance.

DZ twins have 30% concordance.

Heritability is 0.76.

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9
Q

What are some candidate genes?

A

Precursor a.a’s
Receptor genes
Metabolic enzymes
Non-DA sys genes

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10
Q

What have been the genetic findings?

A

High heritability related to multiple common gene variants of small effect size

Rare mutations bestow higher risk

ADHD genomic variants are non-specific

CNVs overlap are also non specific.

ENVIRONMENT IS IMPORTANT- SMOKING ACTIVATED HIGH RISK ALLELES.

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11
Q

What is the fronto-striatal / executive function hypothesis?

A

Executive function is top down control of behaviour.

Impulse control, orient to salient stimuli, flexible strategy, planning, suppress inappropriate actions in favour of appropriate ones.

Tested with stroop test.

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12
Q

What is shown in imaging of the prefrontal cortex?

A

MRI:
Decreased size
Cortical thickness- delay in development by 2-3 years.

Functional imaging:
Less activity on fMRI during EF tasks, less blood low in SPECT.

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13
Q

What is the down-top alternative hypothesis?

A

Prefrontal cortex receives signalling from other structures.

Posterior parietal cortex signals to prefrontal C when completing stimuli require prioritisation towards one stimulus attribute or location.

Decreased blood flow in PPC in ADHD.

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14
Q

What are the function of the BG and cerebellum?

A

Learn to predict events and detect irregularities.

Learn what to expect and when.

Signal to prefrontal C when an unexpected or competing events occurs at an unexpected time.

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15
Q

Is it down top or top down dysfunction?

A

ADHD is a diverse range of EF and non EF deficits.

Pathological & aetiological heterogeneity likely.

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16
Q

Which receptors are supposedly risky alleles?

A

DRD4 receptor

DAT1

17
Q

What is the management of ADHD?

A

-Assessment
(psychiatrist)

-Psycho-education
(explain disorder, info leaflets, educate/liase with school)

-Behavioural
(realistic expectations, praise/reward, clear rules, keep calm, quality time, naughty step)

-Meds
Can be used if ongoing problems despite environmental modification
Methylphenidate, Dexamfetamine, Lisdexamfetamine

18
Q

How do stimulants wor?

A

Readdress pathological underactivity by increasing synaptic DA. Competitively blocks DAT, agonist on D4R.

Not easily abused because it clears striatum slower than cocaine, and oral dosing take longer.