Conditions Flashcards
(48 cards)
What is ADHD?
There is a normal spectrum amongst children and adults in their level of activity throughout the day and night, and their ability to concentrate on a single task for an extended period.
Attention deficit hyperactivity disorder (ADHD) is at the extreme end of “hyperactivity” and inability to concentrate (“attention deficit“). It affects the person’s ability to carry out everyday tasks, develop normal skills and perform well in school.
Features should be consistent across various settings. When a child displays these features only at school but is calm and well behaved at home, this is suggestive of an environmental problem rather than an underlying diagnosis.
What are the features of ADHD?
All the features of ADHD can be part of a normal spectrum of childhood behaviour. When many of these features are present and it is adversely affecting the child, ADHD can be considered:
Very short attention span
Quickly moving from one activity to another
Quickly losing interest in a task and not being able to persist with challenging tasks
Constantly moving or fidgeting
Impulsive behaviour
Disruptive or rule breaking
How is ADHD managed?
A detailed assessment should be carried out by a specialist in childhood behavioural problems before a diagnosis is made. Management should be coordinated by a specialist in ADHD. Parental and child education is essential. This includes education about parental strategies to manage the child eg positive parenting and behaviour techniques - programmes available. In older children, CBT may be helpful.
Establishing a healthy diet and exercise can offer significant improvement in symptoms. Keeping a food diary may suggest a link between certain foods, such as food colourings, and behaviour. Elimination of these triggers should be done with the assistance of a dietician
Medication is an option after conservative management has failed or in severe cases. This should be coordinated by a specialist. Contrary to what you might think, they are central nervous system stimulants. Examples are:
Methylphenidate (“Ritalin“)
Dexamfetamine
Atomoxetine
What changes on what imaging might you see in ADHD?
Positron emission tomography may show decreased function of the frontal lobes and nearby connections
What are the three core diagnostic criteria for ADHD? What do they involve?
- Impulsivity
-Blurts out answers
-Interrupts others
-Cannot take turns
-Intrudes on others
-Poor road safety - Inattention
Often unable to:
-Listen/attend closely
-Sustain attention in play
-Follow instructions
-Finish homework
-Organise tasks needing sustained application
-Loses/forgets things - Hyperactivity
-Squirming/fidgeting
-On the go all the time
-Talks incessantly
-Climbs over everything
-Restless
-No quiet hobbies
What are the differential diagnoses for ADHD?
-Age-appropriate behaviour
-Low or high IQ
-Hearing impairment
-Behavioural disorders
What other conditions might ADHD be associated with?
-Conduct disorder
-Other disruptive behaviour disorders
Young people are at risk of being victims of assault, self-harm and suicide.
Which medications can be given in ADHD and what are their risks?
All CNS stimulants, They increase dopamine and norepinephrine.
- Methylphenidate (Ritalin). Can be given as immediate or modified release. It is recommended to stop the medication at weekends and over the holidays as it can reduce appetite and suppress growth
- Amphetamines eg atomoxetine and dexamfetamine. These take up to 6 weeks to reach full efficacy. The risks are drug misuse/substance abuse due to the street value of amphetamines (speed)
How is serotonin synthesised? How does it activate neurons?
In the presynaptic neurons using the amino acid tryptophan to produce 5-hydroxytryptamine (5-HT), aka serotonin.
They are stored in vesicles until action potential arrives. Serotonin is then released into the synaptic cleft where it binds to 5-HT2 receptors on the postsynaptic neuron to fire an action potential.
On the presynaptic neuron there are serotonin reuptake transporters (SERTs) that allow resorption of serotonin into the presynaptic neuron to reduce the serotonin in the synaptic cleft.
Which are the SSRIs and what is their mechanism of action?
Escitalopram, fluoxetine, fluvoxamine, sertraline, paroxetine and citalopram
They bind to the serotonin reuptake transporters on the presynaptic cleft and inhibit them which increases the serotonin level in the synaptic cleft.
The medications are slow acting as serotonin accumulates (takes 4-6 weeks for effects to be seen).
How is serotonin syndrome treated?
Benzodiazepines and supportive care
Which are the SNRIs?
Duloxetine
Venlafaxine
Which are the TCAs? How do they work?
Amitriptyline
Imipramine
Clomipramine
Inhibit serotonin and norepinephrine transporters to increase the levels of these in the synaptic cleft
(but less selective than SNRIs)
They also block histamine receptors causing sedation, muscarinic receptors causing anticholinergic effects and alpha-1 receptors causing orthostatic hypotension
What is the risk of TCAs with alcohol?
severe respiratory depression
(can also happen with sedatives)
How do MAOIs work?
Once neurotransmitters have been taken back up into the presynaptic neuron, the enzymes monoamine oxidases break down the neurotransmitters.
Inhibiting these increases the level of all the neurotransmitters (serotonin, norepinephrine and dopamine)
Which are the MAOIs?
Non-selective/irreversible:
-Isocarboxazid
- Phenelzine
- Tranylcypromine
(all neurotransmitters)
Selective:
Selegiline
Rasagiline
(only inhibit monoamine oxidase B so only increase levels of dopamine - means they are useful to treat parkinson’s disease)
What is hypertensive crisis and how is it caused?
-Hyperthermia
- High BP
- High HR
- Arrythmias
- Agitation
When MAOIs are combined with tyramine rich foods such as cheese, wine and beer. Monoamine oxidases usually break down tyramines so if they are inhibited there are high levels and this can cause a hypertensive crisis
How do atypical antidepressants work?
Alpha-2 receptors on the presynaptic neuron inhibit the activity of the presynaptic neurons and reduce the release of serotonin and norepinephrine. Drugs that inhibit this neuron reduce the inhibition of the neuron, therefore raising the neurotransmitter release.
Mirtazapine - inhibits alpha-2, selective 5-HT2 and histamine receptors (sedation)
Trazodone & Nefazodone
Vilazodone
Bupropion - inhibits norepinephrine, dopamine and nicotinic receptors
What are the 4 dopamine pathways in the brain? Which are effected in psychotic disorders?
1 - Mesolimbic
Regulates motivation and desire
High levels of dopamine cause the positive symptoms seen in schizophrenia including delusions, hallucinations and disorganised thoughts
2 - Mesocortical
Regulates Emotions
Low levels of dopamine causes the negative symptoms of schizophrenia such as lack of motivation, social withdrawal and flat affect
3 - Nigrostriatal
Motor neurons that bypass the medullary pyramids to control involuntary movements and coordination
4 - Tuberoinfundibular
Releases dopamine to limit the secretion of prolactin
Which are the typical antipsychotics? How do they work?
Haloperidol - high potency
Chlorpromazine - low potency
- They block dopamine D2 receptors in the mesolimbic pathways to alleviate positive symptoms
- However, they block dopamine receptors in the mesocortical pathway which may worsen negative symptoms
- They block the dopamine receptors in the chemoreceptor trigger zone which is responsible for the vomiting reflex, and therefore they can decrease nausea and vomiting
- They block histamine H1 receptors which can have sedative effect
- They also block dopamine in the tuberoinfundibular pathway which can stimulate the release of prolactin, causing oligomenorrhoea, galatctorrhoea and gynaecomastia
- They block dopamine in the nigrostriatal pathways which cause extrapyramidal symptoms eg acute dystonia (eg oculogyric crisis), Akathisia (restlessness), parkinsonism (rigidity, bradykinesia and tremors), tardive dyskinesia (constant, involuntary rhythmic movements eg lip smacking), neuroleptic malignant syndrome
How is neuroleptic malignant syndrome differed from serotonin syndrome?
NMS - Hyporeflexia and normal pupils
SS - Hyperreflexia and dilated pupils
Which are the atypical antipsychotics and how do they work?
Clozapine
Olanzapine
Quetiapine
Risperidone
Aripiprazole
- They block dopamine D2 receptors in the mesolimbic pathways to alleviate positive symptoms
- They block 5-HT2 receptors in the mesocortical pathway which increases dopamine levels and helps relieve the negative symptoms
- They block histamine H1 receptors which can have sedative effect
- They also block dopamine in the tuberoinfundibular pathway which can stimulate the release of prolactin, causing oligomenorrhoea, galatctorrhoea and gynaecomastia (risperidone is the most common to cause these)
- Can cause metabolic syndrome (especially clozapine and olanzapine)
What are the effects of barbiturates and how do they work?
Eg amobarbital, butabarbital, Phenobarbital, thiopental and primidone
These enhance the effects of GABA, the inhibitory neurotransmitter. They increase the duration of the postsynaptic neuron channels opening and therefore increase the levels of Cl- entering the neuron causing hyperpolarisation and therefore difficulty depolarising to fire an action potential, so less responsive to stimuli.
They can be used as anticonvulsants, induce anaesthesia, as anxiolytics and to manage insomnia
What are the effects of benzodiazepines and how do they work?
Enhances GABA, the inhibitory neurotransmitter. They bind to GABA receptors on the postsynaptic neuron to increase the effects of GABA.
Anxiolytics, anticonvulsants, hypnotic for insomnia, anaesthetic and to treat withdrawal symptoms