Pharmacological Interventions Flashcards

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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
Q

Disorders of attention range from what to what?

A

Neurodevelopmental ADHD to those acquired due to stroke, TBI or neurodegenerative disease.

26
Q

Name four symptoms of attention dysfunction.

A

Easily distracted by other stimuli.
Trouble recalling something one has heard or read.
Trouble shifting attention efficiently.
Trouble focusing on a task.

27
Q

The frontoparietal-predominant network is involved in attention. Name the three regions of this network.

A

Parietal cortex.
Frontal cortex.
Cingulate gyrus.

28
Q

Name the five NTs associated with attention.

A

GABA.
Acetylcholine.
Serotonin.
Dopamine.
Noradrenaline.

29
Q

Describe the NTs that may be involved in ADHD.

A

There may be a disruption in NT transporter systems, leading to depleted levels of dopamine and noradrenaline.

30
Q

What is the role of catecholamines in attention?

A

They are responsible for modulating attentional tone. Appropriate levels help improve the signal of processed information to attend to and inhibit potential distractors.

31
Q

Why is methylphenidate/ritalin used for ADHD and narcolepsy treatment?

A

It is thought to block the reuptake of noradrenaline and dopamine into presynaptic neurons.

32
Q

What occurs in the prefrontal cortex during states of hyperarousal or hyperactivity?

A

Excessive glutamatergic transmission.

33
Q

How does memantine or amantadine help to improve attention during states of hyperarousal?

A

It blocks glutamatergic NMDARs.

34
Q
A