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Psychopharmacology > Chapter 11: ADHD > Flashcards

Chapter 11: ADHD Flashcards

1
Q

what CSTC pathway modulates the ability to sustain attention

A

from the DLPFC to the striatal complex

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2
Q

what causes symptoms of inattention in ADHD such as inability to finish tasks, disorganization, and trouble sustaining mental effort

A

inefficient information processing in the DLPFC

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3
Q

what CSTC loop pathway modulates selective inattention and inability to focus

A

CSTC loop from dorsal anterior cingulate cortex to striatal complex, then thalamus, back to dorsal anterior cingulate cortex

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4
Q

inefficient activation of which pathway leads to deficits in selective attention like not listening, losing things, focusing, making careless mistakes

A

CSTC loop from the dorsal anterior cingulate cortex to striatal complex, thalamus, and back to dorsal anterior cingulate cortex

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5
Q

which CSTC pathway modulates hyperactive symptoms

A

from prefrontal motor cortex to the putanem, thalamus, and back to prefrontal motor cortex

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6
Q

which CSTC loop pathway is associated with impulsive symptoms such as talking excessively, blurting out things, interrupting, and not waiting for one’s turn

A

CSTC loop from the orbital frontal cortex to the striatal complex, thalamus, and back to orbital frontal cortex

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7
Q

what area of the brain is associated with impulsive symptoms

A

orbital frontal cortex

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8
Q

what other psych conditions (common comorbidities) are also associated with the orbital frontal cortex

A

conduct disorder
ODD
bipolar

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9
Q

which areas of the brain are most associated with sustained and selective attention deficits

A

DLPFC and dACC

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10
Q

what area of the brain is most associated with symptoms of impulsivity and hyperactivity

A

alterations in the orbital frontal cortex

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11
Q

what neurotransmitters are associated with regulation of attention and behavior

A

dopamine and norepinephrine

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12
Q

what happens if tonic firing of norepinephrine neurons innervating the PFC is too low

A

problems with cognitive functioning

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13
Q

what happens when norepinephrine levels are too high

A

anxiety, substance abuse, mania, and problems with working memory

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14
Q

what happens with dopamine receptors when tonic firing of dopamine neurons is too low

A

sensitive postsynaptic D3 receptors are stimulated but there is inadequate dopamine to stimulate D1 which causes inadequate downstream neuronal signaling resulting in cognitive dysfunction

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15
Q

How does methylphenidate block NETs and DATs

A

allosterically with no action at VMAT2

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16
Q

how does amphetamine block NET and DAT

A

it is a competitor and pseudo substrate for them. So they bind at the same transport site, preventing the monoamines from binding there

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17
Q

which isomer is more potent for DAT binding

A

D

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18
Q

How does atomoxetine work

A

blocks NETs in the PFC which increases both dopamine and norepinephrine

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19
Q

what is the minimum threshold of DAT occupancy required for therapeutic action in ADHD

A

50-60%

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20
Q

what medication is good for augmenting stimulants when there are oppositional symptoms

A

clonidine

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21
Q

what receptors, located on the spines of cortical pyramidal neurons, can gate incoming signals

A

a2A and D1 in the PFC

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22
Q

how are a2A receptors in the PFC linked to cAMP molecules

A

via an inhibitory G protein (Gi)

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23
Q

how are D1 receptors in the PFC linked to cAMP molecules

A

stimulatory G proteins (Gs)

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24
Q

which type of channel strengthens incoming signals

A

closed

25
Q

what does stimulation of D1 receptors in the PFC lead to

A

weakening of incoming signals

26
Q

how does stimulation of D1 receptors in the PFC open channels to weaken incoming signals

A

when dopamine/agonist binds to D1 it activates the Gs-linked system that results in HCN channel opening leading to signal leakage and shunting input out of the spine

27
Q

what does stimulation of a2A receptors in the PFC do to incoming signals

A

when NE/agonist binds to a2A it activates the Gi-linked system that results in closing the HCN channel allowing the signal through to strengthen connectivity to similar neurons

28
Q

what if the same neuron receives NE input at an a2A receptor on one spine and DA input at a D1 receptor on another spine

A

D1 stimulation can turn down the noise while a2A stimulation can increase the signal resulting in proper PFC functioning

29
Q

what if there is not enough stimulation of both a2A OR D1 receptors

A

increased noise and decreased signal

30
Q

what is the gist of pruning

A

synapses rapidly increase in the PFC until age 6 and then half are eliminated by adolescence (over-produced or weak synapses are eliminated to allow for cognitive maturation)

31
Q

order of comorbid symptom treatment with ADHD

A
  1. substance abuse disorder
  2. mood disorders
  3. anxiety disorders
  4. ADHD
  5. nicotine dependence
32
Q

ADHD can result from what type of levels of NE and DA

A

too high or too low

33
Q

MOA of methylphenidate

A

blocks NETs and DATs allosterically with no action at VMAT2

34
Q

common brand names for methylphenidate DL

A

ritalin
concerta

35
Q

common brand name for methylphenidate D

A

focalin

36
Q

of D and L, which isomer of methylphenidate is more potent for both NETs and DATs

A

D

37
Q

MOA of amphetamine

A

competitive inhibitor and pseudo-substrate for NET and DAT
-binds to the same transporter sites as monoamines, thus inhibiting their reuptake

38
Q

how does amphetamine abuse cause euphoria

A

after competitive inhibition of DAT, amphetamine is transported to presynaptic DA terminals where it is also a competitive inhibitor of VMAT2 for both DA and NE. Once in the synaptic vesicles DA there is displaced causing a flood of DA release. As it accumulates in the presynaptic neuron the direction of DATs is reversed spilling intracellular DA into the synapse. This opens presynaptic channels to further release dopamine into the synapse

39
Q

which amphetamine isomer is more potent for DAT binding

A

D

40
Q

which type of amphetamine has more action on DATs than NETs

A

D-amphetamine

41
Q

D and L amphetamine isomers action on NETs

A

about equal for NET binding

42
Q

DAT and NET binding of mixed salts over D-amphetamine

A

mixed salts have more action on DATs than NETs but still more action at NETs that D-amphetamine

43
Q

how do you attain immediate therapeutic actions by inhibiting DAT

A

DAT occupancy levels above a critical threshold
Minimum threshold for action is 50-60%

44
Q

how does atomoxetine work

A

selective NE reuptake inhibitor

45
Q

blocking NETs in the PFC versus the Nucleus accumbens

A

blocking NET in the PFC increases both DA and NE there. Blocking NET in the nucleus accumbens does not increase DA and NE as there are relatively few NE neurons there. This is why NET inhibitors do not have abuse potential

46
Q

what are some other medications with notable norepinephrine reuptake inhibition

A

wellbutrin
desipramine
nortriptyline

47
Q

where is the highest concentration of a2A receptors

A

cortex
locus coeruleus

48
Q

what do a2A receptors mediate

A

NE effects in the PFC (regulates sx of inattention, hyperactivity, and impulsivity)

49
Q

location with the highest concentration of a2B receptors

A

thalamus

50
Q

which receptor is important in mediating the sedating effects of NE

A

a2B

51
Q

where are a2C receptors densest

A

striatum

52
Q

opposing actions of a2 and a1

A

-when NE is low a2 mechanisms at the synapse predominate
-when NE is high a1 mechanisms at synapses predominate

53
Q

which adrenergic receptors are guanfacine most selective for

A

a2A

54
Q

guanfacine v. clonidine for sedation and BP reduction

A

10x weaker than clonidine for sedation but more potent at enhancing PFC function

55
Q

what else is guanfacine approved for

A

augmentation for patients with oppositional symptoms

56
Q

clonidine selectivity for a2 receptors

A

relatively nonselective with action at a2A, a2B, and a2C

57
Q

off label indications for clonidine

A

conduct disorder
ODD
tourette’s

58
Q

when is clonidine good for augmenting stimulants

A

when there are oppositional symptoms

Psychopharmacology (13 decks)

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