Week 4 - ADHD and ASD Flashcards

1
Q

Dopamine systems for ADHD

A

Mesocrticolimbic dopamine
Mesostriatal dopamine
VTA area

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2
Q

ADHD neurotransmitters

A

Dopamine
Noradrenaline - Locus Coeruleus - aplha and beta receptors
Less d and n

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3
Q

Noradrenaline and Dopamine

A

Control glutamate and gaba neurons in their terminal areas

ADHD - signal is noisy

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4
Q

What areas of the brain are eratic in ADHD

A

PFC and NA

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5
Q

How do ADHD treatments work?

A

enhance the amount of time that dopamine or noradrenaline is in the synaptic cleft - less eratic firinig

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6
Q

How do medications work?

A

Re-uptake (transporter) antagonists
Ritalin etc

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7
Q

How do dexamphetamine work?

A

Blocks dopamine and noradrenaline by reversing their function (stops uptake and also increases release of catecholamines via the transporter)

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8
Q

Other therapies - how does guanfacine and clonidine work?

A

Agonists at A2 receptors - activates noradrenaline neurons of locus coreclueus and directly acts on A2 receptors in PFC - creates EPSP

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9
Q

Neuropathology of ASD

A

Shorter cerebellum (PFC)
Increased density of smaller neurons in:
Amygdala
Cortex
Hippocampus

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10
Q

Epigenetics of ASD

A

Histones - positively charged proteins that interact and bind with the acid and negatively charged DNA molecule

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11
Q

How does Phenylketonuria cause ASD?

A

Inability to break P down to tyosine(maqke dopamine)
P inhibits myelination of neurons

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12
Q

What is the opiod excess theory?

A

Gluten and Caesin cross BBB if not metabloised and activate opiate receptors

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13
Q

Serotonergic dysfunction in ASD

A

Increased seratonion in periphery
High levels cause negative feedback (5hT1a) on seratonin cells and loss of terminals

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14
Q

Anxiety and obsessive behaviour treatment in ASD

A

SSRI’sA

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15
Q

Aggression treatment

A

Atypical antipsychotics

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16
Q

hyperactivity treatment

A

ADHD stimulants

17
Q

TICS treatment

A

A2 agonists (clonidine), antipsychotics

18
Q

Seizures treatment

A

AnticonvulsantsS

19
Q
A