ADHD Flashcards

1
Q

Working memory describes

A

what is actively being considered at any moment

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2
Q

Working memory is associated with

A

the prefrontal cortex and the parietal lobes

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3
Q

Working memory is modulated by the catecholamines:

A

dopamine (DA) and norepinephrine (NE).

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4
Q

Why are adolescents so impulsive and prone to taking risks?

A

One possible explanation is that the frontal cortex has not yet matured

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5
Q

Problems with selective attention are believed to be linked to inefficient information processing in the

A

dorsal anterior cingulate cortex (dACC)

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6
Q

problems with sustained attention are linked to inefficient information processing in the

A

dorsolateral prefrontal cortex (DLPFC).

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7
Q

Hyperactivity may be modulated by the

A

prefrontal motor cortex

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8
Q

impulsivity may be modulated by the

A

orbitofrontal cortex (OFC).

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9
Q

. Sustained attention is hypothetically modulated by

A

a cortico-striato-thalamo-cortical (CSTC) loop

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10
Q

Sustained attention is involves

A

involves the dorsolateral prefrontal cortex (DLPFC) projecting to the striatal complex

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11
Q

Inefficient activation of this can lead to difficulty following through or finishing tasks, disorganization, and trouble sustaining mental effort?

A

DLPFC (Dorsolateral prefrontal cortex)

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12
Q

Inefficient activation of this can result in symptoms such as paying little attention to detail, making careless mistakes, not listening, losing things, being distracted, and forgetting things

A

dACC dorsal anterior cingulate cortex

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13
Q

Impulsivity is associated with?

A

a cortico-striato-thalamo-cortical (CSTC) loop that involves the orbitofrontal cortex (OFC), the striatal complex, and the thalamus.

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14
Q

These are examples of what ADHD symptom? talking excessively, blurting things out, not waiting one’s turn, and interrupting.

A

Impulsivity

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15
Q

Motor activity, such as hyperactivity and psychomotor agitation or retardation, can be modulated by

A

a cortico-striato-thalamo-cortical (CSTC) loop from the prefrontal motor cortex to the putamen (lateral striatum) to the thalamus and back to the prefrontal motor cortex

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16
Q

If stimulation at alpha-2A and D1 receptors is too low, all incoming signals are the same, making

A

it difficult for a person to focus on one single task (unguided attention).

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17
Q

If stimulation is too high (right side) at alpha-2a and D1, incoming signals get jumbled as additional receptors are recruited, resulting

A

in the misdirection of attention.

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18
Q

ADHD is an out-of-tune

A

prefrontal cortex

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19
Q

Alterations within the orbitofrontal cortex (OFC) are hypothesized to lead to

A

problems with impulsivity or hyperactivity.

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20
Q

Inadequate tuning of the DLPFC or the dACC can respectively lead to

A

sustained or selective attentive symptoms

21
Q

aberrations in the dorsolateral cognitive network have been observed in children with problems of

A

sustained attention.

22
Q

Salience-provoked phasic firing will lead to bursts of DA release, and when this happens in a controlled manner it can

A

reinforce learning and reward conditioning, which can provide the motivation to pursue naturally rewarding experiences

23
Q

When the salience-provoked phasic firing that leads to bursts of DA release is hijacked

A

reward circuitry can be hijacked, and impulses are followed by the development of uncontrolled compulsions to seek drugs.

24
Q

What are the two types of agents that will be hypothetically beneficial in patients with ADHD by bringing prefrontal activity back to optimal level.

A

Agents that can lead to (1) increased release of these two neurotransmitters, or (2) increased tonic firing of these neurons

25
Q

How does pruning relate to the potential development of ADHD

A

Incorrect pruning that occurs around 6 or 7 may reduce the development of executive function. This is the age many kids are diagnosed with ADHD.

26
Q

Parietal lesions can cause a neglect syndrome in which patients

A

ignore objects, people, and even parts of their body to one side of the center of gaze.

27
Q

Inconsistencies in performance, responding too fast or too slow, and procrastination are behaviors that may be impaired due to

A

temporal processing deficits

28
Q

What tends to have a smaller volume in those with ADHD?

A

Cerebellum volume

29
Q

Most stimulants act by enhancing

A

neuronal excitation

30
Q

At usual doses Amphetamines

A

increase wakefulness and alertness, reduce fatigue, elevate mood, and augment self-confidence and initiative. Euphoria, talkativeness, and increased motor activity are likely. Task performance that had been reduced by fatigue or boredom improves.

31
Q

How do amphetamines affect appetite, respirations, and pain?

A

decrease appetite, stimulate respirations, suppress pain response

32
Q

By a mechanism that is not understood, amphetamines can enhance the

A

analgesic effects of morphine and other opioids

33
Q

Norepinephrine acts in the heart to

A

increase heart rate, atrioventricular conduction, and force of contraction.

34
Q

. Excessive cardiac stimulation

A

can cause dysrhythmias. In blood vessels, NE promotes constriction. Excessive vasoconstriction can cause hypertension

35
Q

Adverse effects of stimulants

A

weight loss, insomnia restlessness, and cardiovascular effects

36
Q

Excessive amphetamine use can result in

A

paranoid psychosis, characterized by hallucinations and paranoid delusions. Amphetamine-induced psychosis looks very much like schizophrenia

37
Q

If withdrawal of amphetamines does not immediately remove psychosis what should be suspected

A

latent schizophrenia

38
Q

Acute Toxicity in amphetamines

A

Overdose produces dizziness, confusion, hallucinations, paranoid delusions, palpitations, dysrhythmias, and hypertension. Death is rare.

39
Q

Fatal overdose is associated with

A

convulsions, coma, and cerebral hemorrhage.

40
Q

In addicts abusing methamphetamines they are finding higher incidences of

A

Parkinson’s disease

41
Q

ADHD improvement with stimulants are generally

A

short term

42
Q

Amphetamines work by

A

reuptaken into the DA terminal andpackaged into vesicles, displacing DA

43
Q

Methylphenidate basically freezes

A

the transporter in time, preventing DA reuptake and thus leading to increased synaptic availability of DA.

44
Q

Unlike amphetamine, methylphenidate is

A

not itself taken up into the DA terminal via the transporter.

45
Q

Treatment with a selective alpha-2A agonist would lead to

A

increased signal via direct stimulation of postsynaptic receptors, resulting in increased ability to sit still and focus.

46
Q

Atomoxetine

A

Therapeutic effects without abuse potential

NE reuptake blocker in nucleus accumbens

47
Q

Guanfacine

A

Prefrontal cortex, not nucleus accumbens

Highly selective for alpha-2A

48
Q

Clonidine

A

Prefrontal cortex, not nucleus accumbens
Less alpha-2A selective than guanfacine
More sedation and hypotension
Off label for ADHD