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PHS 931 > Block 4 Lecture 2 -- ADHD > Flashcards

Block 4 Lecture 2 -- ADHD Flashcards

1
Q

What have been the most significant developments for ADHD drugs in the past 10 years?

A

drug formulation (LA, ER)

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2
Q

How do males and females differ in ADHD presentation, referral, diagnosis?

A

males:

    • 6-10x more likely to be referred
    • more externalizing behaviors
    • 3x more likely to be diagnosed
    • more likely to have co-morbid neuropsychiatric issues
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3
Q

What CNS “pathways” are involved in attention?

A

1) Alerting pathways
2) orienting pathways
3) working memory pathways
4) executive control pathways

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4
Q

What regions are involved in CNS alerting pathways?

A

1) locus coeruleus
2) HT
3) PFc
4) parietal cx
5) reticular activating system in the brainstem

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5
Q

What regions are involved in CNS orienting pathways?

A

1) parietal cx
2) visual cx
3) auditory cx

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6
Q

What is the function of the locus coeruleus?

A
    • NE synthesis
    • ANS control center

involved in the CNS alerting pathways

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7
Q

What regions are involved in the CNS executive control pathways?

A

1) PFc
2) limbic area
3) basal ganglia
4) cerebellum

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8
Q

What regions are involved in the CNS working memory pathways?

A

1) PFc
2) cingulate cx
3) entorhinal cx
4) hippocampus
5) Amygdala

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9
Q

What is the function of CNS orienting pathways?

A

1) tune spatiotemporal representation of relevant sensory stimuli
2) increase focus on a specific stimulus

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10
Q

What is the function of CNS working memory pathways?

A

process and focus info about sensory stimuli or tasks

– over seconds to mins

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11
Q

What is the function of the executive control CNS pathways?

A

integration and organization of information

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12
Q

What genes are HYPOTHESIZED (not proven) to be mutated/involved in ADHD?

A

1) DAT
2) D4/D5 DAr
- - exon 3 7-repeat allele yields blunted response to DA
3) DBH

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13
Q

What are the theories for ADHD pathology?

A

1) genetic

2) DA deficiency hypothesis

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14
Q

What is the basis for the DA deficiency hypothesis?

A

1) stimulants work for 80% of pts
2) some imaging studies show DA/DAr deficits
3) animal studies support DA’s role in motor control, attention, and impulsivity

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15
Q

What is the basis for the genetic theories of ADHD?

A

one of the most heritable neuropsychiatric conditions!

– 3-8x higher incidence if a parent has ADHD

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16
Q

What are the weaknesses of the DA deficiency hypothesis?

A

1) literature doesn’t support one theory for ALL parts of ADHD
2) literature doesn’t support co-morbidities solely due to DA deficit

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17
Q

What are risk factors for ADHD?

A

1) heredity
- - most significant!
2) labor/delivery complications
3) sub-optimal family environment
4) in utero tobacco smoke or lead exposure
5) developmental drug/alcohol exposure
- - NOT directly caused by bad parenting, tv, etc.

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18
Q

What are co-morbidities of ADHD?

A

1) cigarette smoking
2) conduct disorder
3) bipolar disease
4) depression, anxiety, OCD
5) learning disabilities
6) tourettes
7) sleep disturbances
8) sensory dysfunction
9) pervasive disorders (Asbergers)

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19
Q

What are the most common co-morbidities of ADHD?

A

1) learning disabilities! (40%)
2) conduct disorder (25%)
- - males much more than females
3) bipolar (10%)

tourettes (40-80% of tourettes pts have ADHD)

cigarette smoking is 2-3x the age-adjusted rate
– as symptoms increase, more likely to smoke

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20
Q

What are the 3 presentations of ADHD?

A

1) primary inattention
2) primary hyperactivity/impulsivity
3) combined inattention and hyperactivity/impulsivity

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21
Q

What are the possible diagnoses for a patient with symptoms?

A
    • mild, moderate, or severe
    • primary inattention, primary hyperactivity/impulsivity, or combined

– +/- autism spectrum disorder

presentation can vary across years

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22
Q

How did DSM-IV differ from the current DSM-V?

A

1) presentations called “subtypes”
2) sxs had to appear before 6 yo
3) no mild/mod/severe
4) no ASD co-diagnosis
5) no differences for older patients

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23
Q

What is the Vanderbilt ADHD diagnostic parent rating scale?

A

a tool that differentiates oppositional-defiant disorder, conduct disorder, and anxiety/depression from ADHD

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24
Q

MoA of methylphenidate:

A

blocks DAT and NET

– DAT moreso than NET

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25
Q

What kind of system is methylin ER? What are counseling points?

A

methylcellulose polymer / wax matrix;

    • 8 hour release
    • swallow whole
    • may still require BID admin

(same as ritalin SR)

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26
Q

What kind of system is ritalin SR? What are counseling points?

A

intermediate-acting

methylcellulose polymer / wax matrix;

    • 8 hour release
    • swallow whole
    • may still require BID admin

(same as methylin ER)

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27
Q

What kind of system is Metadate CD/ER? What are counseling points?

A

intermediate-acting

IR/ER bead mixture

    • CD is caps, ER is tabs
    • can open and sprinkle on food
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28
Q

What kind of system is Ritalin LA? What are counseling points?

A

intermediate-acting

IR/ER beads formulated in SODAS

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29
Q

What are the short-acting forms of MPH?

A

1) MPH – Ritalin, Methylin

2) Dex-MPH – Focalin

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30
Q

What are the intermediate-acting forms of MPH?

A

1) Methylin ER, Ritalin SR
- - methylcellulose/wax polymer matrix
2) Metadate ER, Metadate CD
- - ir/er beads
3) Ritalin LA
- - sodas

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31
Q

What are the long-acting forms of MPH?

A

1) Concerta
- - OROS
2) Focalin XR
- - sodas
3) Daytrana TD patch
4) quillivant XR
- - ER liquid MPH

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32
Q

What is SODAS?

A

spheroidal oral drug absorption system

    • outer polymer dissolves, holes form
    • GI fluid enters
    • drug solubilizes and escapes
33
Q

What is OROS?

A

osmotic-release oral system

    • outer immediate release core
    • water enters thru semi-permeable membrane
    • osmotic pressure pushes layers of ensuing ER drug solution out of laser-drilled hole
34
Q

Describe ER liquid used in quillivant XR.

A

20% true soln; 80% ionic exchange resin suspension

35
Q

What kind of system is concerta? Counseling points?

A

OROS

    • 12 hour release
    • QD dosing
36
Q

What kind of system is Focalin XR?

A

SODAS

37
Q

What kind of system is Quillivant XR? Counseling Points?

A

ER liquid ion exchange resin

– QD dosing

38
Q

What is the MoA of amphetamines?

A

1) act on VMAT to reverse DAT
2) decrease MAO activity
- - DA affected moreso than NE

39
Q

What are the short-acting amphetamines?

A

1) Dextroamphetamine and amphetamine salts (Adderall)

2) Dextroamphetamine (Dexedrine, Dextrostat)

40
Q

What are the long-acting amphetamines?

A

1) Dexedrine spansule
2) Adderall XR
3) Lisdexamfetamine (Vyvanse)

41
Q

What kind of system is Dexedrine spansule?

A

IR/ER bead mixture

42
Q

What are the considerations for short-acting amphetamines?

A

1) best for initial treatment!
2) 2-3 x/day dosing :(
3) approved for kids 3+

43
Q

What are the considerations for long-acting amphetamines?

A

worse effects on:

    • evening appetite
    • sleep
    • growth stunting
44
Q

What are the considerations for Vyvanse (also a long-acting amphetamine)?

A

1) delayed onset in therapeutic action

2) less abuse and diversion potential

45
Q

Describe PK of lisdexamfetamine.

A
    • hydrolyzed to d-amphetamine during first pass
  • — in intestines or liver
  • — Lys is cleaved
    • rate-limited biotransformation
46
Q

Describe PK of MPH.

A

t1/2 = 3-4 hr

BID dosing

47
Q

How does dexmethylphenidate compare to methylphenidate?

A

lower dosage

48
Q

In what ages are short-acting MPH and amphetamines approved?

A

MPH: 6+
amphetamines: 3+

49
Q

You’re starting an ADHD patient on psychostimulant therapy. How do you do this?

A

1) titrate slow
- - want efficacy at lowest possible dose to avoid ADRs
2) don’t pick an SR form
- - difficult for titration
- - variable PK
- - variable time to max efficacy

50
Q

When are psychostimulants contraindicated?

A

1) bipolar disorder
2) schizophrenia
3) aggression
- - more DA worsens manic-depressive switching, and schizo and aggressiveness
4) h/o drug/EtOH abuse

51
Q

What are ADRs of psychostimulants?

A

1) black box: sudden death in children
2) diminished appetite, weight loss
3) delayed sleep onset / insomnia
4) late-day “wear off”
5) increased HR and BP
6) irritability, obsessiveness, social withdrawal

52
Q

How to manage appetite and sleep effects of psychostimulants?

A 
appetite/weight loss
-- wears off over time
-- time meals to correlate with minimal med effect
insomnia
-- change dose/formulation
-- follow sleep hygiene
53
Q

What is the MoA of atomoxetine?

A

selective NET inhibitor

54
Q

What are ADRs of atomoxetine?

A

1) dry mouth
2) constipation
3) n/v
4) insomnia
5) sympathomimetic ADRs limit use

55
Q

When is atomoxetine used in ADHD?

A

1) substance abuse
2) stimulant failure or severe ADRs
3) need a 24h solution
- - ex: behavior problems in the am
- - ex: sleep disruption is a problem

56
Q

Why is atomoxetine not first line?

A

lower efficacy than stimulants

57
Q

What a2-adrenergic agonists are available for use in ADHD?

A

1) clonidine (IR/XR)

2) guanfacine (IR/XR)

58
Q

What is the MoA of clondine IR/XR?

A

probably POST-synaptic a2-adrenergic receptors in prefrontal cortex

59
Q

When are a2-adrenergic agonists used for ADHD?

A

NOT first line

1) best for hyperactive/aggressive patients
2) substance abuse
3) severe tics
4) seizure disorders
5) sleep disturbances
6) psychostimulant failure

60
Q

How is clonidine/guanfacine administered for ADHD?

A

1) ER formulations more useful, but still BID

2) can be adjunct to stimulants

61
Q

What are ADRs of clonidine/guanfacine

A

sedation (IR worst)
dry mouth
hypotension

62
Q

What antidepressants are used for ADHD treatment?

A

1) bupropion
2) duloxetine
3) venlafaxine
4) TCAs: imipramine and nortriptyline

NO SSRIs alone, not effective

63
Q

MoA of bupropion:

A

DAT/NET

– also lowers seizure threshold

64
Q

MoA of duloxetine:

A

SERT/NET

65
Q

MoA of Venlafaxine:

A

SERT/NET

66
Q

MoA of TCAs:

A

DAT/NET/SERT

67
Q

When are antidepressants used for ADHD?

A

maybe for ADHD + depression

– off-label

68
Q

What are the drug classes used for ADHD?

A

1) psychostimulants
2) selective NET inhibitors
3) a2-adrenergic agonists
4) antidepressants

69
Q

What are the effects of pharmacotherapy in ADHD?

How does it compare to counseling vs. the combination?

A

1) lessens sxs, sets stage for CBT benefits
2) continuous improvements
3) may slightly DELAY growth
4) no increase in substance abuse/diversion

– better than counseling; no obvious advantage with the combo

70
Q

What are the non-drug treatments of ADHD?

A

1) personal and family education
2) lifestyle changes
3) assistance in educational settings
4) improving interpersonal relationships
5) improving health habits
- - sleep, exercise, eating

71
Q

What are the DSM-V requirements for ADHD diagnosis in kids?

A

6 signs of inattention or hyperactivity for ≥ 6 mos

    • must appear before age 12
    • 2 settings
    • 2 independent evaluators
72
Q

What are the DSM-V requirements for ADHD diagnosis in adults?

A

5 signs of inattention or hyperactivity for ≥ 6 mos

    • child-onset, persistent, and current sxs
    • usually have significant sxs
    • 2 settings, 2 evaluators
73
Q

How does ADHD change with age?

A

decreased hyperactivity and impulsivity

persisting inattention

74
Q

What is DA’s supposed role in ADHD treatment?

A

decreasing inappropriate system “noise”

75
Q

What is NE’s supposed role in ADHD treatment?

A

increasing appropriate signaling

76
Q

What things lead to sudden onset disorders resembling ADHD?

A

1) head trauma
2) stroke
3) prefrontal cortex damage

77
Q

What is the thought for pathophysiology behind ADHD?

A

defects in one of the brain attention pathways

– specific neurochemical deficits are difficult to identify

78
Q

How is impulsivity studied?

A

delayed discounting

– presence of impulsive choice associated with gambling, risky behaviors, etc.

79
Q

What is the underlying pathophys of impulsivity?

A

damage to PFc DA system

PHS 931 (29 decks)

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