Pharmacological Interventions Flashcards

1
Q

Define disorders of arousal (DOA).

A

A group of sleep-related behaviours that occur when a person doesn’t fully transition out of non-rapid eye movement (NREM) sleep.

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2
Q

Name three causes of DOA.

A

Hypoxic-ischemic brain injury.
Traumatic brain injury (TBI).
Severe metabolic disturbances.

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3
Q

Disorders of consciousness are found at one extreme of the DOA spectrum. Name three examples of this.

A

Coma.
Minimally conscious state (MCS).
Persistent vegetative state (PVS).

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4
Q

What is the neuroanatomic pathway typically implicated in DOA?

A

Ascending reticular activating system (ARAS).

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5
Q

Name four types of neurons that are found in the ARAS.

A

Noradrenergic.
Cholinergic.
Dopaminergic.
Glutamatergic.

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6
Q

What are two medications that are used to treat DOAs?

A

Amantadine.
Zolpidem.

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7
Q

What does amantadine specifically treat?

A

Improves functional outcomes in altered consciousness following severe TBI.

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8
Q

What does zolpidem specifically treat?

A

Improves functional recovery from coma.

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9
Q

Executive dysfunction can be divided into four categories. Name them.

A

Working memory.
Inhibition.
Set-shifting.
Fluency.

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10
Q

Define working memory.

A

The ability to temporarily store and manipulate information, which allows for longer-term information storage.

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11
Q

Give an example of a working memory deficit.

A

Not being able to remember why you’ve entered a room.

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12
Q

Define inhibition.

A

The adaptive ability to control automatic or previously learned responses to certain stimuli in service of a goal at hand.

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13
Q

Give an example of an inhibition deficit.

A

Interrupting others frequently in conversation.

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14
Q

Define set-shifting.

A

The ability to adapt one’s behaviour or thoughts in response to a changing environment.

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15
Q

Give an example of a set-shifting deficit.

A

Finding it difficult to solve a problem that requires multiple, different steps.

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16
Q

Define fluency.

A

The ability to generate verbal and visual information.

17
Q

Give an example of a fluency deficit.

A

Feeling slow in one’s thinking or speech.

18
Q

Name four regions that are part of the neuroanatomy of executive function.

A

Prefrontal cortex.
Parietal lobe.
Basal ganglia.
Cerebellum.

19
Q

Define processing speed.

A

The speed and efficiency of information transfer in the brain.

20
Q

Processing speed may be predominantly subserved by what?

A

Distributed white matter tracts in the brain.

21
Q

Name five conditions that may slow processing speed.

A

MS.
TBI.
Stroke.
Carbon monoxide exposure.
Inflammatory conditions.

22
Q

Which drug type improves executive function in PD dementia patients?

A

Cholinesterase inhibitors.

23
Q

Which drug type improves executive function in children and adults with ADHD?

A

Psychostimulants.

24
Q

Which drug improves executive function in patients with depression?

A

Vortioxetine (SSRI and mixed serotonin agonist/antagonist).

25
Disorders of attention range from what to what?
Neurodevelopmental ADHD to those acquired due to stroke, TBI or neurodegenerative disease.
26
Name four symptoms of attention dysfunction.
Easily distracted by other stimuli. Trouble recalling something one has heard or read. Trouble shifting attention efficiently. Trouble focusing on a task.
27
The frontoparietal-predominant network is involved in attention. Name the three regions of this network.
Parietal cortex. Frontal cortex. Cingulate gyrus.
28
Name the five NTs associated with attention.
GABA. Acetylcholine. Serotonin. Dopamine. Noradrenaline.
29
Describe the NTs that may be involved in ADHD.
There may be a disruption in NT transporter systems, leading to depleted levels of dopamine and noradrenaline.
30
What is the role of catecholamines in attention?
They are responsible for modulating attentional tone. Appropriate levels help improve the signal of processed information to attend to and inhibit potential distractors.
31
Why is methylphenidate/ritalin used for ADHD and narcolepsy treatment?
It is thought to block the reuptake of noradrenaline and dopamine into presynaptic neurons.
32
What occurs in the prefrontal cortex during states of hyperarousal or hyperactivity?
Excessive glutamatergic transmission.
33
How does memantine or amantadine help to improve attention during states of hyperarousal?
It blocks glutamatergic NMDARs.
34