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Spring 2024 Therapeutics 3 > Exam 4 ADHD > Flashcards

Exam 4 ADHD Flashcards

1
Q

When the body first receives sensory or internal milieu input, where does it go?

A

Brainstem Reticular Formation

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2
Q

Ultimately, where does all sensory input end up going? (This place mediates conscience)

A

Cerebral Cortex

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3
Q

What are two possible causes of ADHD in early life?

A

-Low birth weight

-Fetal alcohol syndrome

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4
Q

What is the main implicated system in ADHD?

A

Dopamine transporters

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5
Q

What is the main physiological goal of ADHD treatment?

A

Increase brain activity by causing more action potentials to fire

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6
Q

What classifications must someone meet to be diagnosed with ADHD?

A

6 or more symptoms present
(for adults 17 and older, 5 symptoms are required)

Several inattentive or hyperactive symptoms must be present prior to age 12

Significant impairment in two or more settings

*Interferes with functioning and development

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7
Q

What is a possible circuity mechanism of ADHD?

A

Medial Prefrontal Cortex (mPFC) may not be fully developed

*this brain region is important for inhibition of impulsive thoughts
*not fully formed during childhood and suppressed with alcohol

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8
Q

What are methylxanthines and how do they work?

A

Indirect-Acting Sympathomimetics

-stimulants that mimic the effect of endogenous agonists of the sympathetic nervous system (fight or flight)

*stimulate the brain and make it more active

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9
Q

What substance is considered a stimulant and has a similar structure to the stimulant meds?

A

Caffeine

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10
Q

What are the 3 actions of methylxanthines?

A

-Antagonize Adenosine Receptors
(naturally produced by brain, quiets body down and slows heart rate, block this to increase alertness)

-Inhibit Phosphodiesterases
(increase cAMP)

-Increase Activity of Ryanodine Receptors
(Increase intracellular Ca)

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11
Q

How does Adenosine work?

A

-Enhances exocytosis of glutamate so there is less, this quiets the system down

-Opens the K channels so it exits the cell, this hyperpolarizes the cell and quiets it down

want to block this

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12
Q

Which G protein is the adenosine receptor A1 linked to?

A

Gi/o

(i=inhibitory)

*Inhibits modulation of many neurotransmitters

*Causes sedation/quieting down

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13
Q

Activation of adenosine receptor A1 causes what?

A

CNS: Sedation, Anxiolysis, Anticonvulsant Activity

Peripheral: Decreased heart rate

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14
Q

Adenosine A2A receptors are linked to which G protein?

A

Gs

(s=stimulatory)

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15
Q

Activation of Adenosine A2A receptors leads to what?

A

Vasodilation

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16
Q

Adenosine A2B receptors are linked to which G-protein and where are they found*?

A

Gs-linked

*Glial cells

(unknown function)

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17
Q

When are Adenosine A3 receptors activated?

A

Excessive catabolism

(seizures, hypoglycemic stroke)

*Not antagonized by methylxanthines

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18
Q

What are the two main functions of methylxanthines?

A

Increase alertness

Decrease fatigue

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19
Q

How does Cocaine affect norepinephrine?

A

Directly blocks the norepinephrine transporter (NET)

-this blocks NE reuptake
-there is an excessive amount of NE in the extracellular space, makes person feel very energized

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20
Q

How do amphetamines affect norepinephrine?

A

-Can be up taken by norepinephrine transporters (NET)

*Bind VMAT

-This confuses the transporters and they start pumping out more dopamine and NE

-Higher levels of these extracellularly increase alertness and reduce fatigue

Amphetamines act as mimics of NE and reverse transport to outside of the cell

NO DIRECT BLOCKING

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21
Q

What does VMAT stand for?

A

Vesicular Monoamine Transporter

*note: these package NE and dopamine into transport vesicles

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22
Q

What is a downside of using stimulants?

A

Target many reward pathways, potential for abuse

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23
Q

What is the primary monoamine affected by stimulants?

A

Dopamine

*also NE

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24
Q

What is the pharmacology of stimulants?

A

Monoamine transporters

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25
Q

What is an example of an indirect acting sympathomimetic?

A

Cocaine

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26
Q

Cocaine inhibits monoamine transporters that transport which substances?

A

Norepinephrine (NE)
Serotonin (5-HT)
Dopamine (DA)

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27
Q

What medical use does cocaine have?

A

Local anesthetic

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28
Q

Which receptor is targeted by MDMA (molly/ecstasy)?

A

5-HT

*research use shows it may increase sociability, researching use in autism

“Psychedelic Revival”

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29
Q

What ideas are fueling the “psychedelic revival”?

A

-Psychedelics target 5-HT
-May increase sociability/have use in autism
-Not considered as dangerous as other hard drugs

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30
Q

What is the difference between amphetamines and methamphetamines?

A

Methamphetamines are hard drugs with an extra methyl group that allows them to more easily cross the BBB

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31
Q

What are the Amphetamine drugs?

A

-Dextroamphetamine (Dexedrine)
-Lisdexamfetamine (Vyvanse)
-Methylphenidate (Ritalin)
-Dexmethylphenidate (Focalin)
-Adderall
-Mydayis

32
Q

What are amphetamines used for?

A

-Narcolepsy
-Anorexiant/Weight loss
-ADHD

33
Q

What are the non-stimulants used for ADHD?

A

-Atomoxetine (NET reuptake inhibitor for adults)
-TCAs
-Bupropion
-Clonidine/Guanfacine

34
Q

What is Modafinil used for?

A

Narcolepsy

*not ADHD

35
Q

Whay are the drugs used to treat narcolepsy?

A

-Stimulants
-Solriamfetol
-Modafinil
-Antidepressants
-Xyrem
-Pitolisant

36
Q

What are stimulants used for regarding narcolepsy?

A

To treat sleepiness

37
Q

What is Solriamfetol used for?

A

Treatment of Obstructive sleep apnea and Narcolepsy Excessive Sleepiness

(TONES)

38
Q

What is the MOA of Solriamfetol?

A

NET and DAT inhibitor

39
Q

What is the MOA of Pitolisant?

A

Histamine 3 (H3) receptor antagonist

40
Q

When does a person have a higher chance of being diagnosed with ADHD?

A

If a first-degree relative has it

41
Q

What is the etiology of ADHD?

A

Multifactorial

-environmental
-genetics
-physiological

42
Q

What fraction of children diagnosed with ADHD will continue to have it in adulthood?

A

1/3

43
Q

What are two co-morbid conditions that have an increased risk in people with uncontrolled ADHD?

A

-Substance use
-Antisocial personality disorder

44
Q

How long does it take to see the effects of stimulants?

A

Short period of time

45
Q

How do we dose stimulants?

A

DO NOT DO WEIGHT BASED DOSING IN PEDIATRIC PATIENTS (variations are not weight-based)

IR preferred for patients <16kg (limited low-dose availability of long-acting stimulants)

Late afternoon symptoms may require longer-acting forms

46
Q

When should stimulants be taken?

A

Early in the day, avoid giving dose too late

*may give an after-school dose if afternoon symptoms

47
Q

When would we use two different stimulants?

A

NEVER

-can use two different dosage forms of the same stimulant though

48
Q

Which medication is only used in age 13-17?

A

Mydayis

49
Q

Which medication has a patch formulation?

A

Daytrana

50
Q

Which medication is a prodrug?

A

Vyvanse

51
Q

What is the prodrug Vyvanse converted to?

A

Dextroamphetamine

52
Q

Which medication should be taken in the evening?

A

Jornay PM

(between 6:30pm and 9:30pm)

53
Q

What are the adverse effects of stimulants?

A

-Appetite loss
-Stomachache
-Headache
-Insomnia
-Decreased growth
-Hallucinations
-Increased BP!
-Increased HR!
-Priapism (sustained erection)
-Raynaud’s
-Irritability/Jitteriness

**Hallucinations (bad)
**Sudden cardiac death (bad, not high risk)

54
Q

What do we want to monitor with stimulants?

A

-Appetite
-Behavior
-BP
-Growth rate
-Heart rate
-Sleep
-ECG (if cardiac risk)

55
Q

What is Guanfacine ER a substrate of?

A

3A4

56
Q

Which medications need to be tapered if discontinued due to rebound hypertension?

A

-Guanfacine
-Clonidine

57
Q

Which medication has weight-based dosing?

A

Atomoxetine

(only up to 70 kg then not weight-based)

58
Q

What is Atomoxetine a substrate of?

A

2D6

59
Q

What is Viloxazine a substrate of?

A

2D6 and UGT

60
Q

What is an important fact to note about Viloxazine?

A

STRONG 1A2 INHIBITOR

61
Q

What differentiates Viloxazine from other medications?

A

Capsules

(can swallow whole or put in applesauce)

62
Q

What are the side effects of Atomoxetine/ Viloxazine?

A

Increased HR and BP

Increased suicidal thinking (boxed warning) *not an antidepressant

63
Q

What are the side effects of Clonidine/Guanfacine?

A

Decreased HR and BP
Orthostasis
Somnolence
Dizziness
Rebound hypertension w/ abrupt discontinuation

64
Q

What do we monitor with non-stimulants?

A

Appetite
Behavior
BP
Growth rate
HR
LFT’s****
Sleep

65
Q

When would we use Bupropion for ADHD?

A

*Not FDA approved for ADHD

-Attractive in the elderly due to increased dopamine and not controlled

-Consider if patient cannot take stimulants

-Not as effective

66
Q

What is Bupropion an inhibitor of?

A

2D6

67
Q

What medication is contraindicated in seizure disorders and eating disorders?

A

Bupropion

68
Q

What are the main concerns with tricyclic antidepressant use for ADHD?

A

-Less effective than methylphenidates
-Cardiac concerns (sudden cardiac death in children, lethal overdose)

69
Q

When would we use mood stabilizers/ atypical antipsychotics for ADHD?

A

If comorbid bipolar disorder, conduct disorder, or intermittent explosive disorder

THESE DO NOT TREAT ADHD

70
Q

What is the ADHD treatment used in preschool age kids?

A

First-line: Parent training in behavior management (PTBM)

Second-Line: PTBM plus medications

71
Q

What is the ADHD treatment used in elementary + middle-school age kids?

A

First-line: FDA-approved meds + PTBM

72
Q

What is the ADHD treatment used in adolescents (age 12-18)?

A

First-line: Meds, may offer PTBM

73
Q

For preschool-age children, what is the first-line medication class used?

A

Methylphenidates

74
Q

For middle school-age kids what is the first- and second-line medications used?

A

First-line: Stimulants
Second-line: Atomoxetine, Guanfacine ER, Clonidine ER

75
Q

Which agents can be used as adjunct treatment in ADHD?

A

Only Guanfacine ER and Clonidine ER

76
Q

Which agents should be used in adults with ADHD?

A

1st: Methylphenidate or Lisdexamfetamine (Vyvanse)

2nd: Dextroamphetamine

3rd: Atomoxetine

Spring 2024 Therapeutics 3 (24 decks)

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