CMN 554 Module 2 Study Guide | Questions with 100% Correct Answers |
Verified | Latest Update - University of South Alabama
Developmental and Childhood Mental Health
Disorders
Treating ADHD
1. Discontinuation syndrome with stimulants
• Abrupt withdrawal after prolonged use may result in dysphoria, irritability or a rebound in symptoms of ADHD; increase in sleep
and appetite reported
• If a stimulant is taken in conjunction with an antipsychotic, sudden discontinuation of the stimulant may result in the emergence of
extrapyramidal symptoms previously masked by the stimulant’s anticholinergic properties and competition for D 2 receptors
• Case of priapism reported in 16-year-old each time he forgot to take his dose of extended-release methylphenidate (Concerta) 54
mg
2. MOA and general principles for atomoxetine
• Mechanism of action:
Selectively blocks the reuptake of norepinephrine; increases dopamine and norepinephrine in the frontal cortex (without increasing
dopamine in subcortical areas) – leads to cognitive enhancement without abuse liability; suggested to be important in regulating
attention, impulsivity, and activity levels.
▪ No stimulant or euphoriant activity – may be advantageous in patients with comorbid substance use disorder
• General comments:
• Most ADHD treatment guidelines list atomoxetine as a second-line agent. May be effective for some patients who have not responded to
stimulant treatment, who have comorbid anxiety, or individuals who have an active comorbid substance use disorder. Benefits include a
lack of euphoria, a lower risk of rebound, a lower risk of induction of tics or psychosis, low abuse potential, and increased somnolence
• Available evidence indicates that stimulants and atomoxetine have both been found to be superior to placebo for reducing the severity of
ADHD symptoms on average in the short term
• Has a slow onset of action and response may take up to 4 weeks – titrate dose gradually to help mitigate adverse effects (especially in
patients who may be poor CYP2D6 metabolizers: ~10% of the population). Response is seen at 4 weeks of full dose and full optimization
of drug response requires at least 3 months
• Ultrarapid metabolizers of CYP2D6 (28% of North Africans, Ethiopians, and Arabs; up to 10% of Caucasians; 3% of African Americans,
and up to 1% of Hispanics, Chinese, and Japanese) would have reduced efficacy of atomoxetine
• Reduces both the inattentive and hyperactive/impulsive symptom clusters of ADHD
• Head-to-head studies show greater reductions in ADHD symptoms (net effect size difference = 0.3) and a greater percentage of responders
with stimulants when compared to atomoxetine
• A large head-to-head trial of OROS-methylphenidate (Concerta) vs. atomoxetine in over 600 children demonstrated that 40% of children
who do not respond to methylphenidate are responders to atomoxetine, indicating a selective response .
3. Nonresponse to treatment strategies
Ascertain whether diagnosis is correct.
▪ Ascertain if patient is adherent with therapy (speak with caregivers, check with pharmacy for late refills, count remaining pills in
container and compare to prescription fill date)
▪ Ensure dosage prescribed is therapeutically appropriate and tailor regimen to have peak serum levels occur at those times of the
day when symptoms are most prominent.
▪ Consider trying a stimulant from an alternate class (methylphenidate class or amphetamine class) if first trial was ineffective and
the patient was adhering to therapy recommendations.
4. Indications for 2 agonists
▪ ADHD (clonidine (Kapvay) and guanfacine (Intuniv/Intuniv XR)) – meta-analysis of studies suggests a moderate benefit in
children and adolescents; reduced hyperarousal, agitation, aggression, impulsivity, and sleep disturbances; useful in patients with
concurrent tic disorders or conduct disorder; minimal benefit on inattentive symptoms
▪ Hypertension (guanfacine – USA only)
▪ Some benefit apparent in combination with stimulants; may help ameliorate sleep disturbances caused by psychostimulants
(Caution – see Drug Interactions p. 310)
▪ May improve behavior or impulsivity when used alone or in combination with methylphenidate (Caution – see Drug Interactions p.
310)
Autism – reported to be effective for reducing hyperarousal and controlling some problematic behaviors in children and adults
Menopausal flushing
,▪ Generalized anxiety disorder (GAD), panic attacks, phobic disorders, and obsessive-compulsive disorders: Of some benefit; may
augment effects of SSRIs and cyclic antidepressants in social phobia; helpful for symptoms of hyperarousal, hypervigilance,
aggression, and irritability of PTSD
May relieve antipsychotic-induced asthenia and improve symptoms of tardive dyskinesia
May help decrease clozapine-induced sialorrhea
, ▪ Heroin, cocaine, and nicotine withdrawal: Used to reduce agitation, tremor, and diaphoresis, and to increase patient comfort.
Opioid antagonists (e.g., naltrexone) as well as dicyclomine (for stomach cramps) and cyclobenzaprine (for muscle cramps) often
given concomitantly
5. Target symptoms for 2 agonists
Both clonidine and guanfacine stimulate ↵ 2 -adrenergic receptors in the brain stem. This reduces sympathetic outflow from the CNS and
decreases peripheral resistance, renal vascular resistance, heart rate, and blood pressure.
6. Treating rebound symptoms from stimulants
The extended-release, sustained-release, or controlled-release formulations may decrease inter dose dysphoria or “wear off” phenomenon
(“rebound” hyperactivity). Supplementation with short-acting preparations may be needed in the morning (to speed up onset) or in the
afternoon (to extend duration of action) for some extended-release preparations with a relatively lower proportion of immediate-release
stimulant such as Concerta (all others are active within 30–60 min)
7. Baseline and Monitoring for patients on stimulants
Baseline: Height, weight, blood pressure, and pulse and repeat regularly throughout treatment. Patients with a prior or family history of
cardiac disease should be further evaluated via ECG and cardiology consult, including echocardiogram as necessary. Cardiac evaluation
recommended if patient experiences excessive increase in blood pressure or pulse, exertional chest pain, or unexplained syncope
8. Treating ADHD medication-induced insomnia
Drug-induced insomnia [can be managed by changing dose timing or formulation based on expected duration of action; addition of
melatonin, sedating antihistamines or trazodone (25–50 mg) at bedtime or clonidine 100 micrograms given 2 h before bedtime. When
stimulants wear off at the end of the day, patient may experience rebound or a period of irritability and return of ADHD symptoms in excess
of baseline – this may cause difficulty in falling asleep
9. Treating comorbid Tic disorder and ADHD
▪ Tic disorders: research investigating increased risk of tics with the use of stimulants has yielded contradictory results. Tics tend to
wax and wane, often independent of therapy, though clinicians have commented that stimulants can unmask tics.
▪ ADHD (clonidine (Kapvay) and guanfacine (Intuniv/Intuniv XR)) – meta-analysis of studies suggests a moderate benefit in children and
adolescents; reduced hyperarousal, agitation, aggression, impulsivity, and sleep disturbances; useful in patients with concurrent tic
disorders or conduct disorder; minimal benefit on inattentive symptoms
Child and Adolescent Development
1. Five developmental domains
There are five (5) developmental domains.
The mnemonic PILES can help to remember them.
Review Sadock (2017) chapters 35.2 and 35.3 for overview of Normal Child and Adolescent Development.
, 2. Erikson’s Eight Stages of the Life Cycle and
concepts in clinical application
Application of Erikson’s Concepts to Clinical Work
Erikson’s view of individual experience as inexorably embedded in developmental, familial, societal, and historical contexts crucially
shaped his ideas concerning mental illness and psychiatric treatment. As noted previously, Erikson was reluctant to pathologize behavior or to rush
to judgment about the meaning of any given symptom. He asserted, “Perhaps there are certain stages in the life cycle when even seemingly
malignant disturbances are more profitably treated as aggravated life crises rather than as diseases subject to routine psychiatric diagnosis.”
To understand the meaning of such “disturbances,” Erikson drew upon his training in classical drive theory (with its concepts of the
unconscious; id, ego, and superego conflicts; repression, regression, and repetition compulsion) but emphasized the adaptive and synthesizing
capacities of the ego in brokering relations between internal drives and external reality. When Erikson listened to his patients, he thought about
their symptoms not simply as compromise formations between libidinal drive and superego prohibition but also as expressions of arrested or
derailed psychosocial development. Toward this end, Erikson examined many aspects of his patient’s current life (e.g., skills, talents, and
aspirations; religious and political commitments; social and intimate relationships; roles as worker, partner/spouse, and parent) and located them
within a larger social, cultural, and historical context. His focus was on the individual’s entire life cycle, the development of specific virtues and
those factors which facilitated or retarded psychosocial growth. As Shapiro and Fromm point out:
He paid attention to the whole life context of any immediate situation. He asked a number of questions. What is the immediate stimulus
for the patient’s reaction? What is the acute life conflict, the current developmental stage, the issues that are manifest? In what developmental
context did the patient’s reaction first occur? Is it now manifest in the relationship to the therapist, in a repetitive conflict, in a characteristic way
that the individual solved earlier developmental struggles? In what social context is the individual embedded, what roles are available?… What
defenses does the individual use? What are the individual’s deepest psychological investments?”
Erikson conceived of these psychological investments in broad terms. He used concepts of attachment, separation, and mutuality (defined
as “a relationship in which partners depend on each other for the development of their respective strengths”) to illustrate ways in which the
individual is essentially a social being. He recognized that psychological crises often occurred at times of developmental separation or
individuation and that fears regarding dependency and abandonment were frequently the catalyst for such crises. Though Erikson acknowledged
the influence of early childhood conflict or trauma on an individual’s progress in negotiating developmental tasks in adolescence and adulthood,
he did not think that the issues being played out were simply reiterations of infantile conflict.
Verified | Latest Update - University of South Alabama
Developmental and Childhood Mental Health
Disorders
Treating ADHD
1. Discontinuation syndrome with stimulants
• Abrupt withdrawal after prolonged use may result in dysphoria, irritability or a rebound in symptoms of ADHD; increase in sleep
and appetite reported
• If a stimulant is taken in conjunction with an antipsychotic, sudden discontinuation of the stimulant may result in the emergence of
extrapyramidal symptoms previously masked by the stimulant’s anticholinergic properties and competition for D 2 receptors
• Case of priapism reported in 16-year-old each time he forgot to take his dose of extended-release methylphenidate (Concerta) 54
mg
2. MOA and general principles for atomoxetine
• Mechanism of action:
Selectively blocks the reuptake of norepinephrine; increases dopamine and norepinephrine in the frontal cortex (without increasing
dopamine in subcortical areas) – leads to cognitive enhancement without abuse liability; suggested to be important in regulating
attention, impulsivity, and activity levels.
▪ No stimulant or euphoriant activity – may be advantageous in patients with comorbid substance use disorder
• General comments:
• Most ADHD treatment guidelines list atomoxetine as a second-line agent. May be effective for some patients who have not responded to
stimulant treatment, who have comorbid anxiety, or individuals who have an active comorbid substance use disorder. Benefits include a
lack of euphoria, a lower risk of rebound, a lower risk of induction of tics or psychosis, low abuse potential, and increased somnolence
• Available evidence indicates that stimulants and atomoxetine have both been found to be superior to placebo for reducing the severity of
ADHD symptoms on average in the short term
• Has a slow onset of action and response may take up to 4 weeks – titrate dose gradually to help mitigate adverse effects (especially in
patients who may be poor CYP2D6 metabolizers: ~10% of the population). Response is seen at 4 weeks of full dose and full optimization
of drug response requires at least 3 months
• Ultrarapid metabolizers of CYP2D6 (28% of North Africans, Ethiopians, and Arabs; up to 10% of Caucasians; 3% of African Americans,
and up to 1% of Hispanics, Chinese, and Japanese) would have reduced efficacy of atomoxetine
• Reduces both the inattentive and hyperactive/impulsive symptom clusters of ADHD
• Head-to-head studies show greater reductions in ADHD symptoms (net effect size difference = 0.3) and a greater percentage of responders
with stimulants when compared to atomoxetine
• A large head-to-head trial of OROS-methylphenidate (Concerta) vs. atomoxetine in over 600 children demonstrated that 40% of children
who do not respond to methylphenidate are responders to atomoxetine, indicating a selective response .
3. Nonresponse to treatment strategies
Ascertain whether diagnosis is correct.
▪ Ascertain if patient is adherent with therapy (speak with caregivers, check with pharmacy for late refills, count remaining pills in
container and compare to prescription fill date)
▪ Ensure dosage prescribed is therapeutically appropriate and tailor regimen to have peak serum levels occur at those times of the
day when symptoms are most prominent.
▪ Consider trying a stimulant from an alternate class (methylphenidate class or amphetamine class) if first trial was ineffective and
the patient was adhering to therapy recommendations.
4. Indications for 2 agonists
▪ ADHD (clonidine (Kapvay) and guanfacine (Intuniv/Intuniv XR)) – meta-analysis of studies suggests a moderate benefit in
children and adolescents; reduced hyperarousal, agitation, aggression, impulsivity, and sleep disturbances; useful in patients with
concurrent tic disorders or conduct disorder; minimal benefit on inattentive symptoms
▪ Hypertension (guanfacine – USA only)
▪ Some benefit apparent in combination with stimulants; may help ameliorate sleep disturbances caused by psychostimulants
(Caution – see Drug Interactions p. 310)
▪ May improve behavior or impulsivity when used alone or in combination with methylphenidate (Caution – see Drug Interactions p.
310)
Autism – reported to be effective for reducing hyperarousal and controlling some problematic behaviors in children and adults
Menopausal flushing
,▪ Generalized anxiety disorder (GAD), panic attacks, phobic disorders, and obsessive-compulsive disorders: Of some benefit; may
augment effects of SSRIs and cyclic antidepressants in social phobia; helpful for symptoms of hyperarousal, hypervigilance,
aggression, and irritability of PTSD
May relieve antipsychotic-induced asthenia and improve symptoms of tardive dyskinesia
May help decrease clozapine-induced sialorrhea
, ▪ Heroin, cocaine, and nicotine withdrawal: Used to reduce agitation, tremor, and diaphoresis, and to increase patient comfort.
Opioid antagonists (e.g., naltrexone) as well as dicyclomine (for stomach cramps) and cyclobenzaprine (for muscle cramps) often
given concomitantly
5. Target symptoms for 2 agonists
Both clonidine and guanfacine stimulate ↵ 2 -adrenergic receptors in the brain stem. This reduces sympathetic outflow from the CNS and
decreases peripheral resistance, renal vascular resistance, heart rate, and blood pressure.
6. Treating rebound symptoms from stimulants
The extended-release, sustained-release, or controlled-release formulations may decrease inter dose dysphoria or “wear off” phenomenon
(“rebound” hyperactivity). Supplementation with short-acting preparations may be needed in the morning (to speed up onset) or in the
afternoon (to extend duration of action) for some extended-release preparations with a relatively lower proportion of immediate-release
stimulant such as Concerta (all others are active within 30–60 min)
7. Baseline and Monitoring for patients on stimulants
Baseline: Height, weight, blood pressure, and pulse and repeat regularly throughout treatment. Patients with a prior or family history of
cardiac disease should be further evaluated via ECG and cardiology consult, including echocardiogram as necessary. Cardiac evaluation
recommended if patient experiences excessive increase in blood pressure or pulse, exertional chest pain, or unexplained syncope
8. Treating ADHD medication-induced insomnia
Drug-induced insomnia [can be managed by changing dose timing or formulation based on expected duration of action; addition of
melatonin, sedating antihistamines or trazodone (25–50 mg) at bedtime or clonidine 100 micrograms given 2 h before bedtime. When
stimulants wear off at the end of the day, patient may experience rebound or a period of irritability and return of ADHD symptoms in excess
of baseline – this may cause difficulty in falling asleep
9. Treating comorbid Tic disorder and ADHD
▪ Tic disorders: research investigating increased risk of tics with the use of stimulants has yielded contradictory results. Tics tend to
wax and wane, often independent of therapy, though clinicians have commented that stimulants can unmask tics.
▪ ADHD (clonidine (Kapvay) and guanfacine (Intuniv/Intuniv XR)) – meta-analysis of studies suggests a moderate benefit in children and
adolescents; reduced hyperarousal, agitation, aggression, impulsivity, and sleep disturbances; useful in patients with concurrent tic
disorders or conduct disorder; minimal benefit on inattentive symptoms
Child and Adolescent Development
1. Five developmental domains
There are five (5) developmental domains.
The mnemonic PILES can help to remember them.
Review Sadock (2017) chapters 35.2 and 35.3 for overview of Normal Child and Adolescent Development.
, 2. Erikson’s Eight Stages of the Life Cycle and
concepts in clinical application
Application of Erikson’s Concepts to Clinical Work
Erikson’s view of individual experience as inexorably embedded in developmental, familial, societal, and historical contexts crucially
shaped his ideas concerning mental illness and psychiatric treatment. As noted previously, Erikson was reluctant to pathologize behavior or to rush
to judgment about the meaning of any given symptom. He asserted, “Perhaps there are certain stages in the life cycle when even seemingly
malignant disturbances are more profitably treated as aggravated life crises rather than as diseases subject to routine psychiatric diagnosis.”
To understand the meaning of such “disturbances,” Erikson drew upon his training in classical drive theory (with its concepts of the
unconscious; id, ego, and superego conflicts; repression, regression, and repetition compulsion) but emphasized the adaptive and synthesizing
capacities of the ego in brokering relations between internal drives and external reality. When Erikson listened to his patients, he thought about
their symptoms not simply as compromise formations between libidinal drive and superego prohibition but also as expressions of arrested or
derailed psychosocial development. Toward this end, Erikson examined many aspects of his patient’s current life (e.g., skills, talents, and
aspirations; religious and political commitments; social and intimate relationships; roles as worker, partner/spouse, and parent) and located them
within a larger social, cultural, and historical context. His focus was on the individual’s entire life cycle, the development of specific virtues and
those factors which facilitated or retarded psychosocial growth. As Shapiro and Fromm point out:
He paid attention to the whole life context of any immediate situation. He asked a number of questions. What is the immediate stimulus
for the patient’s reaction? What is the acute life conflict, the current developmental stage, the issues that are manifest? In what developmental
context did the patient’s reaction first occur? Is it now manifest in the relationship to the therapist, in a repetitive conflict, in a characteristic way
that the individual solved earlier developmental struggles? In what social context is the individual embedded, what roles are available?… What
defenses does the individual use? What are the individual’s deepest psychological investments?”
Erikson conceived of these psychological investments in broad terms. He used concepts of attachment, separation, and mutuality (defined
as “a relationship in which partners depend on each other for the development of their respective strengths”) to illustrate ways in which the
individual is essentially a social being. He recognized that psychological crises often occurred at times of developmental separation or
individuation and that fears regarding dependency and abandonment were frequently the catalyst for such crises. Though Erikson acknowledged
the influence of early childhood conflict or trauma on an individual’s progress in negotiating developmental tasks in adolescence and adulthood,
he did not think that the issues being played out were simply reiterations of infantile conflict.
