PBL - ADHD Flashcards

1
Q

When does brain remodelling occur and end?

A

It happens intensively around adolescence and continues into the mid 20s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is grey matter in the brain highest?

A

Early adolescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens to the nerve cells age children age?

A

They get coated in myelin, increasing connectivity and affects how well different parts of the brain work together.
So there is an increase in white matter in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why are teenagers more likely to engage in impulsive and risky behaviour that adults?

A

Because the emotional amygdala has become fully developed, but the frontal cortex (responsible for keeping the emotional impulses in check) is still in maturity.
Also, the brain is still making synapses, refining brain pathways and myelinating axons. This means coordinated thought, action and behaviour are still developing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why are teens more likely to be self-concious?

A

Hormones changes in the brain increases oxytocin production.

There is increased sensitivity to this in the limbic system, and it is linked to self-consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens to the cortical grey matter in development?

A

It is pruned, and only the paths that we use often are retained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Summarise what happens during adolescent brain development.

A
CSF volume increases
Cortex size decreases
Cortical grey matter thins
Increased white matter - myelinations
Increased ventricle size
Reduced number of neurons and connections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two categories that the clinical features of ADHD can be split into?

A

Inattentiveness

Hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the inattentiveness symptoms of ADHD.

A

Short attention span
Careless mistakes
Forgetful or losing things
Can’t stick at tedious or time consuming tasks
Doesn’t listen or carry out instructions
Constantly changes activity
Has difficulty organising tasks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List the hyperactivity/impulsiveness symptoms of ADHD.

A
Can't sit still 
Fidgeting 
Unable to concentrate on tasks
Excessive physical movement 
Excessive talking
Unable to wait for turns
Acts without thinking
Interrupts conversations
Little/no sense of danger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms of ADHD in adults?

A
Carelessness
Lack of attention
Always starting and nerve finishing tasks
Lack of organisation 
Mood swings/anger
Impatient 
Forgetful 
Excessive risk taking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the co-morbidities associated with ADHD in children?

A
Anxiety
Depression
Oppositional defiant disorder
Sleep problems
Autism
Epilepsy 
Tourettes
Learning difficulties
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the possible genetic causes of ADHD?

A

DRD4 receptor - associated with hyperactivity and impulsivity
DAT1 - dopamine transport gene
DRD5 - dopamine receptor gene
5HTT - serotonin transport gene, associated with volatile emotions
HTR1B - serotonin receptor gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the organic factors of ADHD?

A

Smaller brain volume - especially in the frontal and parietal cortex
Smaller basal ganglia
Reduced right dorso-lateral prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List risk factors for ADHD.

A
Parents have it 
Genetics
Premature baby - low birth rate 
Brain damage in early life
Alcohol/drugs/smoking while pregnant
Exposure to toxins at a young age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Briefly describe the pathophysiology of ADHD.

A

It’s a deficiency in the arousal mechanism
A defective inhibitory response found in a compromised pre-frontal cortex
- neurons in the PFC are out of tune, and cant filter the important external signals from the background noise
- all signals seem the same, causing lack of focus on any one thing
- insufficient information processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the hypo-arousal mechanism of ADHD.

A

Defective inhibitory response
Low tonic firing of dopamine/noradrenergic neurons
Treated with stimulants to amplify tonic firing rates

18
Q

Describe the hyper-arousal mechanism of ADHD.

A

Excess noradrenergic/dopamine stimulates receptors and causes signals to noise detection to deteriorate
Associated with increased phasic firing of NA/D neurons
Treated by down-regulating neuronal activity and desensitise postsynaptic receptors

19
Q

Describe some requirements for a diagnosis of ADHD to be made.

A
  • apparent before the age of 7
  • excessive for age and development
  • pervasive
  • symptoms worse in the afternoon
20
Q

What are the SIGN guidelines for ADHD?

A

The core ADHD symptoms have a significant impact on the development of the child (impairs social, emotional and cognitive functioning)
Symptoms are responsible for morbidity and dysfunction of the child, peers and family

21
Q

Name some things that should be recorded when taking a history of someone with suspected ADHD.

A
Current behaviour, activity levels, impulsivity, emotional reactivity
Ability to sustain interest/attention
Impact on child and family
Interactions with others
Eating and sleeping habits 
Parental management strategies
22
Q

Name some of the things you should record in regards to medical history when examining someone with suspected ADHD.

A
Illness/infection
Operations
Head injury
Hearing problems
Tics/funny turns/faints/fits 
Current medication 
Allergies
23
Q

What is the pharmacological treatment for ADHD?

A

1st line - psychostimulants (methylphenidate and dexamphetamine)
2nd line - atomoxetine
3rd line - clonidine

24
Q

Describe the mechanism of action of dexamphetamine.

A

Blocks dopamine and noradrenaline membrane transporters, thus preventing re-uptake by pre-synaptic neurons
Also travels into the neuron and once inside it prevents noradrenaline/dopamine storage in vesicles
- increases cystolic concentrations and is transported back out into the synaptic cleft

25
Q

What are the side effects of dexamphetamine?

A
Reduced sleep and appetite 
Abdominal discomfort 
Headaches
Hypertension
Tachycardia
26
Q

Describe the mechanism of action of methylphenidate

A

Blocks dopamine transporter molecules, increasing extra-cellular dopamine in striatum
This reduces D2/3 dopamine receptor availability and increases dopamine binding to the remaining receptors

27
Q

What are the side effects of methylphenidate?

A
Reduced sleep and appetite
Abdominal discomfort 
Headaches 
Hypertension
Tachycardia
28
Q

Describe the mechanism of action of atomoxetine

A

Long acting
Selective inhibition of the pre-synaptic noradrenaline transporter (noradrenaline re-uptake inhibitor)
Enhances noradrenaline transmission in the prefrontal cortex area

29
Q

What are the side effects of atomoxetine?

A
Nausea/vomiting
Excessive tiredness
Insomnia 
Abdominal pain/appetite suppression
Constipation
Headaches
Mood swings
Hepatic impairment - monitor LFTs
Increases heart rate/blood pressure
Suicidal intention - raised awareness of parents
30
Q

Describe the mechanism of action of clonidine (alpha adrenergic drug.

A

Short acting
Central and peripheral adrenergic agonists - inhibit noradrenaline at the synapse
Reduces sympathetic output from the CNS and decreases peripheral resistance

31
Q

What are the side effects of clonidine?

A
Sedation
Dizziness
Hypotension - monitor BP
Constipation 
Headaches 
Dry mucosa 
Depression 
Paradoxical hypertension
32
Q

Describe modafinil.

A

A weak psychostimulant
Has a weak affinity for dopamine uptake carrier sites
- decreases GABA and increases glutamate release
- controls degree of hypothalamic arousal
Side effects
- appetite
- abdominal pain
- dry mouth
- tachycardia

33
Q

Describe lisdexamphetamine

A

Increases available dopamine and noradrenaline
Metabolised to dexamphetamine by RBCs at a set rate
Side effects
- same as other stimulants
- dizziness
- drowsiness

34
Q

List the non-pharmacological treatments for ADHD.

A

Psycho-education training for teaching staff
Management of the environment
Behavioural training programme

35
Q

Describe why regular communication is needed between the health and educational services.

A

Promote understanding of the difficulties of ADHD
Consistent approach to patient across all settings
Monitor the effectiveness of interventions

36
Q

Describe the how behavioural training programmes are effective for ADHD treatment.

A

Consistency in behavioural management
Positively reinforce appropriate and acceptable behaviour
Parents need to be firm, but not coercive
Clear rules and consequences
Routines, calendars and reminders
Quiet time, planned ignoring and time-outs
Positive feedback using direct observations of interactions between child and parent

37
Q

Why is management of the environment important in ADHD management?

A

Provides a calm environment with no distracting stimuli
Initially avoids situations which requires quiet and still behaviour for long periods of time
Maintains structure and supervision longer than would be expected to see a permanent result

38
Q

What are the three core features of ADHD?

A

Inattention and lack of persistence
Excessive activity
Impulsivity

39
Q

Describe the progression of tyrosine to dopamine.

A

Tyrosine is converted to DOPA via the action of tyrosine hydroxylase . This is then converted to dopamine via the action of DOPA decarboxylase

40
Q

List some general side effects of psycho-stimulants.

A
Growth retardation 
Anorexia 
BP and HR irregularities 
Insomnia and sleep difficulties 
Sadness
Irritability 
Abdominal pain
Headaches