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AC- CLPT lectures > Pharmacological Management for Autism and ADHD 2.2.1 > Flashcards

Pharmacological Management for Autism and ADHD 2.2.1 Flashcards

1
Q

What are the drugs used for ASD?

A

Risperidone

Glutamatergic drugs

Oxytocin

Fluoxetine

Methyphenidate, atomoxetine (symptoms of ADHD)

Melatonin

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2
Q

What are the drugs used for ADHD

A

Dexamphetamine

Methylphenidate

Atomoxetine

Clonidine

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3
Q

Why are antipsychotics used in ASD?

A
  • Psychotropic drugs cannot cure ASDs but they can reduce the severity of some symptoms.
    *
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4
Q

What drugs are used for the following core symptoms of ASD

A) Restricted repetitive behaviours and interests domain(RRBI)

B) Social and communication impairment domain

C) Inattention, overactivity & impulsiveness in ASD (symptoms of ADHD)

D) Irritability

E) Sleep disturbance

A

A)

  • SSRI = fluoxetine

B)

  • Role of risperidone, glutamatergic drugs and oxytocin

C)

  • Methylphenidate
  • Atomoxetine

D)

  • Risperidone

E)

  • Melatonin
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5
Q

What do all children with autism experience difficulty in?

A

Developing social, speech and behavioural skills.

  • Behavioural therapy is usually first line treatment with pharmacological therapies added to help patients function in their daily activities
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6
Q

MOA of risperidone?

A

Antagonist – D1 and D2 receptor

5-HT2A antagonism enhances or complements D2 receptor antagonism = lower EPS incidence

Antagonism of D3, D4 and other receptors may also contribute to the favourable clinical profile of risperidone

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7
Q

What are the adverse effects of antipsychotics?

A

Adverse effects on Dopaminergic pathways

  • Psychological effects (mesolimbic/mesocortical)
  • Movement disorders (nigrostriatal)
  • Neuroendocrine (tuberoinfundibular)

Blockade of a1 receptors

  • Hypotension, reflex tachycardia

Blockade of histamine H1-receptor

  • Sedation and weight gain

Anti-cholinergic effects

  • Blurred vision, dry mouth, constipation, urinary retention

Adverse effects due to immune reaction

  • Hypersensitivity reactions, dermatitis, rashes, photosensitivity, urticaria

Adverse effects due to individual drug

  • Clozapine cause agranulocytosis - neutropenia, bone marrow depression

Idiosyncratic reaction

  • Neuroleptic malignant syndrome

Most common side effects of risperidone is weight gain, increased appetite, anxiety and fatigue

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8
Q

What is the medical cause of ADHD?

A
  • Genes involved in the regulation of neurotransmitter (NT) catabolism and release have been implicated
  • Dopamine (DA) and noradrenaline (NA) NT systems dysfunction is important for onset, progression and tmt response
  • Certain regions of brain, rich in dopamine and noradrenaline are structurally altered and functionally different
  • Regions involved in visual spatial and verbal attention, working memory and impulse control = ↓ abilities in children affected with ADHD
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9
Q

What are the drug treatments used for ADHD?

A
  • Psychostimulants (methylphenidate and dexamphetamine)
  • Atomoxetine
  • Clonidine
  • TCA’s (imipramine)
  • Neuroleptics
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10
Q

What are the psychostimulants for treatment of ADHD?

A
  • Dexamphetamine
  • Methylphenidate
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11
Q

How do dexamphetamine and methylphenidate help with ADHD?

A

Thought to be equally effective

> dexamphetamine = higher affinity for NA receptors

> methylphenidate = higher affinity for dopamine receptors

  • Immediate and dramatic improvement in impulsive behaviour
  • Less effective in managing aggressive behaviours
  • Have similar range and incidence of adverse effects
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12
Q

What are the mechanism of action of psychostimulants?

A

↑ functional activity of DA and NA by:

  • Inhibiting their pre-synaptic uptake
  • Increase release of dopamine, NA & serotonin

> Help compensatory brain neural networks which promote more cognition, behaviour and emotions

> Effects are dose dependent for hyperactivity and impulsiveness.

> Attention and working memory improve at low doses but can be impaired at high doses

  1. Amphetamine enters the nerve terminal via the NA transporter
  2. Amphetamine will then enter synaptic vesicle via the VMAT (vesicular monoamine transporter) in exchange for NA
  3. Some NA is degraded by MAO and some escapes, in exchange for amphetamine via the NA transporter
  4. The released NA will act on the postsynaptic receptors
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13
Q

Compare dexamphetamine and amphetamines? Long or shorter doa compared to methylphenidate

A

Amphetamine has both dextro- and levoisomers

> Dexamphetamine - greater CNS action and less peripheral action = active dextro isomer of amphetamine

> Has slightly longer duration of effect than methylphenidate

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14
Q

CIR AE of Dexamphetamines?

A

Common

  • Headache – Nausea – ↓appetite – Anxiety – Insomnia – Dry mouth – Tachycardia – Palpitations – Changes in BP (↑ adults)

Infrequent

  • Movement disorders – Tics – Rash – Weight loss – Growth retardation

Rare

  • Pyschosis and liver dysfunction
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15
Q

For methylphenidate:

A) What are its effects

B) What does large doses do

C) What are its properties

A

A)

  • Mild CNS stimulant
  • More effects on mental rather than motor activities

B)

  • Larger doses can over stimulat CNS –> convulsions
  • Pharmacological properties similar to amphetamine

C)

  • Similar to amphetamine
  • Readily absorbed –> peak plasma conc after 2 hours
  • Can be taken every day of the week with a break on weekends
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16
Q

Why is methylphenidate controlled release formulation used? Which patients get PBS-authority?

A

One daily dosing for ADHD

  • Eliminates need for in school and after school dosing
  • Efficacy lasts for 12 hours
  • Minimal potential for abuse

PBS-Authority for ADHD patients who

  • have a demonstrated response to immediate release methylphenidate
  • have not experience any adverse effects
  • require continuous coverage over 12 hours
17
Q

CIR AE of methylphenidate (similar to dexamfetamine)

A

Common

  • insomnia – ↓ appetite = weight loss – nausea – Anxiety – Irritability – Dry mouth – Tachycardia – Palpitations – Changes in BP (↑adults)

Infrequent

  • – Movement disorders – Tics – Rash – Growth retardation

Rare

  • Psychosis – Neuroleptic malignant syndrome – Liver dysfunction
18
Q

Precautions and contraindications for dexamphetamine and methylphenidate?

A

Substance abuse- CI

Active psychotic disorders- CI

Tx with or within 14 days of stopping MAOI’s-CI

Tic disorders or Tourette’s syndrome-may worsen, monitor, consider other Tx e.g. clonidine or atomoxetine.

Angina, arrhythmia,↑BP, hyperthyroidism, glaucoma, anxiety, agitation, phaeochromocytoma- may worsen __> caution especially in patients who are children, especially those on anticoagulants, anticonvulsants and TCAs

Structural cardiac abnormalities –> caution

19
Q

For atomoxetine (used in ADHD)

A) What is its MOA?

B) Compare it to psychostimulants

C) Metabolism

D) Precautions

A

A)

  • Selectively inhibits presynaptic noradrenaline reuptake in CNS
  • Increase noradrenaline and dopamine in pre-frontal cortex and nucleus accumbens therefore low potential for abuse = not a psychostimulant

B)

  • Longer duration of action than psychostimulants
  • Subsidised by PBS for patients who cannot take psychostimulants
  • Well absorbed orally
  • Not possible to confirm whether atomoxetine is as efficient or as well tolerated as the psychostimulants

C)

  • Metabolised by CYP2D6 in liver and excreted through the kidneys
  • CYP2D6 prone to genetic polymorphism thus poor metabolisers of atomoxetine may occur
  • Poor metabolisers show 4 fold ↑ in mean elimination half life

D)

  • Tx with or within 14 days of stopping MAOI- CI
  • Closed angle glaucoma- CI
  • History of seizures-caution when starting
  • Hypertension, tachycardia, cerebrovascular disease- ↑ BP and heart rate
  • Structural cardiac abnormalities- assess risk factors
20
Q

CIR AE of atomoxetine?

A

Common

– N, V – Abdominal pain – Dyspepsia – ↓ appetite – Dry mouth – ↑BP – Dizziness – Somnolence – irritability

Infrequent

Palpitations and tachycardia

Rare

– Suicidal thoughts and behaviours

– Hepatic dysfunction

21
Q

Drug interactions of atmoxetine?

A
  • Risk of serotonin syndrome when atomoxetine is administered with other drugs that raise serotonin levels.
  • Thus avoid combining atomoxetine with drugs that raise serotonin levels e.g. SSRI’s
  • Potent CYP2D6 inhibitors e.g. fluoxetine and paroxetine ↓ metabolism of atomoxetine
22
Q

Why is imipramine used for ADHD

A

TCA

> third line tx for ADHD

> virtually phased out of routine practice

> increase potential for adverse cardiac effects such as cardiac arrhythmias

23
Q

Why is clonidine used in ADHD? How does it work? Which patients to avoid in?

A

Central adrenergic alpha 2 agonist →

↓ presynaptic release of noradrenaline

Used when other options are ineffective or CI

↓ hyperactivity, impulsiveness symptoms more than inattention at low doses •

Some evidence shows improved attention at higher dose

In Australia clonidine is more commonly prescribed with a psychostimulant than alone

DONT USE IN CHILDREN WITH HISTORY OF DEPRESSION –> worsens depression

AE = dry mouth and sedation

24
Q

When to use antipsychotics for ADHD?

A

Atypical antipsychotics e.g. risperidone and sedative antipsychotics e.g. pericyazine are of limited benefit on core ADHD symptoms

BUT they can be beneficial if there is severe aggression or irritability or affective disability

Specialist consultation is required

AC- CLPT lectures (27 decks)

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