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Pharmacology > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

Psychiatric Disorders: also known as… grouped as… and etiology

A
  • Also known as schizophrenic disorders
  • Group of syndromes presenting as massive disruption in thinking, mood, and overall behavior, as well as poor filtering of stimuli
  • Causes are multifactorial
  • Genetic, environmental, neurotransmitter
  • May have familial trait
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2
Q

Psychosis: definition, associations

A

=Major emotional disorder associated with perceptual and functional impairment
May be associated with
-Medications, especially anticholinergics
-Depression, dementia, schizophrenia
-Traumatic event (functional psychosis)
-Organic psychosis related to infection (delirium), poisoning, tumor, hypoxia, injury
-Toxic psychosis: drug/ETOH withdrawal

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3
Q

Schizophrenia: etiology

A

-Pathophysiology unclear
Genetic component: probably a mutation
-Dopamine (DA) theory: excess DA in limbic system, and/or limbic system is hyperresponsive to DA
Frontal cortex becomes hyporesponsive
Possible decreased dopamine type 1 (D1) activity
Other neurotransmitter issues: gamma-aminobutyric acid (GABA), glutamate, serotonin
-Brain structure abnormal related to birth trauma, fetal environment, substance abuse
-Other theories: involvement of excitatory NT, 5HT, ACh, GABA, and NMDA

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4
Q

Classifications of Schizophrenia:

A

Classified in two categories
-Positive symptoms: hallucinations, delusions, formal thought disorders
Thought to be related to increased dopaminergic (D2) activity in the mesolimbic region
-Negative symptoms: diminished socialization, restricted affect, poverty of speech
Thought to be related to decrease in dopaminergic (D3) activity in the mesocortical system

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5
Q

Schizophrenia: SX (positive, negative, cognitive, and miscellaneous)

A
  • Positive symptoms: agitation, delusions, hallucinations, feelings of unreality, racing thoughts, paranoia, and hyperactivity
  • Negative symptoms: amotivation, anhedonia, flat affect, apathy, emotional withdrawal, and poor rapport
  • Cognitive symptoms: attention deficits, memory deficits, lack of judgment or insight, slowed thought processing, and “word salad”
  • Other types: catatonia and paranoid
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6
Q

Schizophrenia: onset and prodrome

A

-Onset: often adolescence
-Prodrome: almost a year long, with subtle changes
Mood changes and inattention
Affects day-to-day functioning as a result of fragmented thoughts

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7
Q

Antipsychotic medications

A
  • Treatment is multimodal: case management, behavioral counseling (but medications are helpful)
  • Most agents block dopamine type 2 (D2) receptor, but some also regulate glutamate (a NT)
  • Used to quiet symptoms and permit improved functioning
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8
Q

Antipsychotics: risks of EPS higher with…

A

-Higher risk extrapyramidal syndrome (EPS) with typical antipsychotics than atypicals

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9
Q

Antipsychotic Meds: Neuroleptic Malignant Syndrome

A 
Neuroleptic malignant syndrome (NMS)
=Life threatening, 
*presents as fevers as high as 107 degrees
*Diaphoresis, 
*rigidity, stupor, coma, 
*acute renal failure
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10
Q

Antipsychotic Meds: Extrapyrimidal Syndrome/ SX and TX

A

Extrapyramidal syndrome (EPS)
=Most common and troublesome
-Pseudoparkinsonism: shuffling, drooling, pill rolling, akathisia, restlessness, dystonia, tardive diskinesia
-Treated with antiparkinson, antihistamine, and anticholinergics

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11
Q

Antipsychotic Meds: other SEs

A
  • Weight gain
  • Photosensitivity
  • Decrease in seizure threshold
  • Orthostatic hypotension
  • Sexual dysfunction
  • Galactorrhea
  • Amenorrhea
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12
Q

Typical Antipsychotics: most effective in TX for and drug interactions

A
  • Wide range of drug-to-drug interactions
  • Potentiate HTN effect of antihypertensive
  • Potentiate effect of anticholinergics
  • More effective in treating symptoms associated with positive than those with negative
  • More effective in treating severe psychosis (patients who are agitated and dangerous)
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13
Q

Prescribing Antipsychotics- initiation, maintenance, RX in elders

A
  • Usual high dose to decrease agitation, then taper
  • Patients respond differently to these medications: “not one fits all”
  • Patients need maintenance dose (high relapse rate if decreased)
  • In elders, avoid prescribing antipsychotics for agitated dementia (prefer mood stabilizers)
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14
Q

Typical Antipsychotics: MOA, examples, and uses

A 
Typical (first generation, neuroleptics)
=Block dopamine D2 receptors
Chlorpromazine (Thorazine)
Thioridazine (Mellaril)
Thiothixene (Navane)
Haloperidol (Haldol)
-Used in acute agitation: most common use in hospital setting or in severe nausea and vomiting (Thorazine)
-Used in dementia, BPD, pre-op sedation (Thorazine), Tourette's, Huntington's chorea
Typicals: high risk of EPS
Atypicals: lower risk of EPS
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15
Q

Risk of EPS: typical vs. atypical antipsychotics

A

Typicals: high risk of EPS
Atypicals: lower risk of EPS

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16
Q

Atypical Antipsychotics: examples

A 
Atypical (second generation)
Clozapine (Clozaril)*
Olanzapine (Zyprexa)*
Risperidone (Risperdal)**
Quetiapine (Seroquel)
AirPiprazole (Abilify)**
Ziprasidone (Geodon)
Asenapine (Saphris)
* Not as commonly used

** Used in pediatric patients

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17
Q

Atypical Antipsychotics: used in PEDS

A

Risperidone (Risperdal)**

AirPiprazole (Abilify)**

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18
Q

Antipsychotics: other uses

A
  • Can be used for acute agitation, dementia, and bipolar disorder
  • Thorazine may be used for acute nausea, vomiting, hiccups, and preoperation sedation
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19
Q

How Antipsychotics work

A
  • Block postsynaptic D2 receptors
  • In mesolimbic area: reduce positive symptoms
  • In medulla and GI tract: antiemesis
  • In basil ganglia: extrapyramidal symptoms
  • Movement disorders: acute dystonia (involuntary muscle spasms), parkinsonism, perioral tremor, neuroleptic malignany syndrome, tardive dyskinesia (involuntary movements mouth, tongue, extremities), and akathisia (restlessness)
  • Reduce positive symptoms
  • Difficult to treat negative and cognitive symptoms
  • To reduce seizure threshold, may need to increase in seizure medication
  • Block ACh receptors: anticholinergic effects (dry mouth, orthostasis, sedation, weight gain)
  • Block alpha adrenergic receptors: orthostastic hypotension
  • Block histamine receptors: sedation and weight gain
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20
Q

Neuroleptic Malignant Syndrome: S/S and mortality

A
  • Tremor
  • Catatonia and stupor
  • Labile pulse and BP; fever to 107
  • Hyperthermia
  • Elevation of creatine kinase (CK)
  • Myoglobinemia
  • Mortality ~10%
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21
Q

Antipsychotics: adverse effects

A

-Allergic dermatitis (macular/papular rash, urticaria), photosensitivity
-Neuroendocrine effects
Amenorrhea
Gynecomastia (rare)
-Hematologic effects: more common with atypicals
Leukopenia, agranulocytosis, leukocytosis
-Cardiovascular effects: arrhythmias

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22
Q

Antipsychotics: withdrawal effect

A

Withdrawal effect: H/A, N/V, salivation, insomnia, and diarrhea

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23
Q

Antipsychotics: in pregnancy??

A

*All have pregnancy concerns (EPS in newborns)

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24
Q

Atypical Antipsychotics- examples with MOA

A

No evidence better than typicals
-Clozapine: block D4, S2, and alpha-2 receptors
Used for treatment resistance
-Olanzapine: block D4, D1, muscarinic, alpha-1, H1 receptors
Most weight gain or metabolic effects, not recommended
-Risperidone: block D2, S2, alpha-1, alpha-2, and H1 receptors
Others: arpiprazole and ziprasidone

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25
Q

Atypical Antipsychotics- controls ____ SX? Effects which NTs? Risk for EPS?

A
  • Aid in controlling negative symptoms as well as positive
  • Have indirect effect on serotonin as well as dopamine
  • Less extrapyramidal syndrome (EPS)
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26
Q

Adverse Reactions in Atyipcal Antipsychotics

A

-Less risk of EPS
-More risk of hematological effects (agranulocytosis)
-Sedation
Olanzapine: anticholinergic effects
*Caution in elders: increases mortality
*All are pregnancy Category C, except clozapine (Category B)
Clozapine: high-risk agranulocytosis, weekly CBC (stop if WBC is less than 3500)

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27
Q

How to choose and antipsychotic: Agitated dementia and Elderly

A

-Depends on patient and cause of psychosis
-Delirium: haloperidol, risperidone
Start low
-Agitated dementia, but off label
Risperidone 0.5–1.5 mg/day
-Elders
First generation: greater risk EPS
Second generation: increased CV events and death

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28
Q

How to choose and antipsychotic: Schizophrenia and Mania

A

Schizophrenia
Ziprasidone (Geodon) or aripiprazole (Abilify)
Second generation, less EPS, less metabolic SEs
Mania (bipolar)
Consult for aripipazole (Abilify) and mood stabilizer (lithium or valproic acid)

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29
Q

Major adverse reactions/ risk of Clozapine (atypical):

A
  • *Clozapine: use should be reserved for severe schizophrenia
  • Can cause fatal agranulocytosis
  • Both patients and provider need to be registered
  • Need a baseline CBC before starting and then up to 4 weeks once drug is discontinued
  • Need to assess for leukopenia, fever, chills, lethargy
  • Agranulocytosis is fatal within 24 to 72 hours
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30
Q

Monitoring and Pt Education on antipsychotics:

A
  • Baseline labs: CBC, LFT, EKG
  • *Weekly WBC if on Clozapine
  • Stigma of psychiatric illness and ADEs
  • For patients on short-term antipsychotics for treatment of vomiting, there is a risk of acute dystonia
  • Education: medication risks/benefits and side effects
  • Always forewarn patients and their family members of potential side effects to maintain trust.
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31
Q

How to TX adverse effects in antipsychotics:

A

Managing SE and EPS

  • Akathisa: BBs may be helpful
  • Parkinsonian S&S
  • Rx with benztropine (Cogentin)
  • Diphenhydramine (Benadryl), antihistamine with anticholinergic properties
  • Amantidine (Symmetrel), a dopamine agonist
  • Discontinuing mediation
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32
Q

Mood Disorders: definition, prevalnce

A

=Mood: a pervasive and sustained emotion that, in the extreme, markedly affects the person’s perception of the world and the ability to adequately function in society
=Mood disorders: when a mood disturbance is combined with associated symptoms that impair the individual’s ability to function
-True prevalence unknown
-Peak: age 25 to 44 and may be increasing in prevalence

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33
Q

Mood disorders: predisposing factors

A

Predisposing factors: family history (first-degree relatives are up to three times more likely), female gender

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34
Q

Depression DX

A

Diagnosis of depression: mood, anhedonia, significant with weight loss or gain, insomnia or hypersomnia, increased or decreased activity

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35
Q

Types of Depression:

A

Depressive disorders

  • Major or minor depressive disorder
  • Dysthymia
  • Seasonal affective disorder
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36
Q

Bipolar disorders: definition

A

Bipolar disorders

=Associated with depression and mania or hypomania

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37
Q

Depression: associated with which NTs, and initial DX usually with….

A
  • Symptoms of depression reflect changes in brain monoamine neurotransmitters: NE, serotonin (5-HT), and dopamine (DA)
  • Initial episodes of depression are more likely to be associated with major life events
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38
Q

Theories of Depression physiology:

A

Theories regarding etiology: NE, DA, 5-HT
1) Biologic amine hypothesis
Depression caused by insufficient amounts of monoamine neurotransmitters or receptor dysfunction: Mostly NE, but also serotonin, and dopamine
2) Permissive hypothesis
Low levels of serotonin permit depressive state
3) Dysregulation hypothesis
Erratic levels of neurotransmitters
5-HT* or NE link hypothesis

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39
Q

Classes of antidepressants:

A

1) Serotonin reuptake inhibitor or 5HT1A receptor partial agonist: Vilazodone (Viibryd)
2) Serotonin reuptake inhibitors (SSRIs)
3) Serotonin-norepinephrine reuptake inhibitors (SNRIs)
Venlafaxine (Effexor)
Desvenlafaxine (Pristique)
Duloxetine (Cymbalta): also neuropathic pain
Milnacipran (Savella): fibromyalgia
4) Mixed reuptake and neuroreceptor antagonists (Tricyclics: TCAs)
Amitriptyline (Elavil)
5) Monoamine oxidase inhibitors (MAOIs)
Phenelzine (Nardil)
Decreases metabolic inactivation of catecholamines
Many side effects and drug-to-drug interactions
6) Serotonin receptor antagonists
Mirtazapine (Remeron), trazodone, and nefazodone
Antidepressant and antianxiety: alpha-2 antagonist
Fewer side effects than tricyclics
7) Aminoketone: bupropion (Wellbutrin)
Weak inhibitor of neuronal uptake of dopamine, NE, and serotonin
8) Atypical antipsychotics
Abilify

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40
Q

Serotonin Reuptake Inhibitor/ 5HT1A Receptor Partial Agonist- example

A

1) Serotonin reuptake inhibitor or 5HT1A receptor partial agonist: Vilazodone (Viibryd)

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41
Q

SSRI’s- examples

A
  • Zoloft (sertraline)
  • Paxil (paroxetine)
  • Celexa (citalopram)
  • Lexapro (escitalopram)
  • Luvox (fluvoxamine)
  • Prozac (fluoxetine)
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42
Q

SRNI’s- examples

A

3) Serotonin-norepinephrine reuptake inhibitors (SNRIs)
Venlafaxine (Effexor)
Desvenlafaxine (Pristique)
Duloxetine (Cymbalta): also neuropathic pain
Milnacipran (Savella): fibromyalgia

43
Q

Tricyclic Antidepressants- example

A

4) Mixed reuptake and neuroreceptor antagonists (Tricyclics: TCAs)
Amitriptyline (Elavil)

44
Q

MAOI’s- example, MOA, caution!

A

5) Monoamine oxidase inhibitors (MAOIs)
Phenelzine (Nardil)
Decreases metabolic inactivation of catecholamines
Many side effects and drug-to-drug interactions

45
Q

Serotonin Receptor Antagonists: examples, MOA, SEs

A

6) Serotonin receptor antagonists
Mirtazapine (Remeron), trazodone, and nefazodone
Antidepressant and antianxiety: alpha-2 antagonist
Fewer side effects than tricyclics

46
Q

Aminoketone: Buproprion (Wellbutrin)-

A

Aminoketone: bupropion (Wellbutrin)

Weak inhibitor of neuronal uptake of dopamine, NE, and serotonin

47
Q

First (usual) choice in antidepressants:

A

SSRI’s

48
Q

SSRI: MOA

A

Actions

  • Potently and selectively inhibit the serotonin uptake pump on presynaptic neuron
  • Increase concentration of 5-HT in synapse by inhibiting reuptake, weak effect on NE and dopamine reuptake
49
Q

SSRI: Indications

A

Indications

  • Often first choice in antidepressants
  • Treatment of anxiety disorders and anxiety complicating depression
  • Obsessive compulsive disorder (OCD)
50
Q

SSRI: Pregnancy Category

A

C!

51
Q

SNRIs: example, MOA, how works at low/ high doses; indications

A

Effexor: serotonin and norepinephrine reuptake inhibitor
Venlafaxine (Effexor)
Actions: dose-dependent sequential effects on the uptake pumps for serotonin and norepinephrine
At lower doses: primarily an SSRI
At higher doses: produces norepinephrine reuptake
Indications: equivalent of adding an NSRI to an SSRI for augmented effects

52
Q

SSRIs: distribution, metabolism (CYP 450?), excretion, T 1/2’s…

A 
-Distribution
Wide Vd
Extensive protein binding
-Metabolism
*Interference with CYP 450 system
-Excretion: renal
-Half-lives vary
Fluoxetine: longest half-life (4–6 days)
Norfluoxetine: half-life (7–10 days)
Fluvoxamine: shortest half-life (15–26 hours)
53
Q

SSRI: SEs

A

Major side effects
-Nausea and loose stools
Mediated by 5-HT3 agonism
-Sexual dysfunction: male and female anorgasmia and decreased libido
Mediated by indirect serotonin agonism and occurs in dose-dependent fashion with all SSRIs and venlafaxine
-Weight gain
**Sexual dysfunction and weight gain are common reasons for discontinuation of SSRIs

54
Q

Serotonin Syndrome: definition and predisposition

A 
Serotonin syndrome
-Increased risk with high dose and combining 5-HT reuptake inhibitors, MAOIs, and St. John's wort, or antiemetics
Rigidity
Hyperthermia
Autonomic instability
Myoclonus
Confusion
Delirium
Coma
*Especially problematic in the elderly
55
Q

Risks of seizures with SSRIs?

A

-Aschenbrenner-patients with history of seizure disorder are at increased risk for seizures with SSRIs

56
Q

Withdrawal Syndrome of SSRI (FLUSH):

A

-Withdrawal syndrome: depressive symptoms or mania
-Withdrawal symptoms = FLUSH
Flu-like, fatigue, myalgia, loose stools, and nausea
Lightheadedness and dizziness
Uneasiness and restlessness
Sleep and sensory disturbances
Headache
-Symptoms remit within 24 hours or restarting SSRI
-Risk factors: time on drug, potency of drug, and half-life

57
Q

Pt monitoring in SSRIs:

A

-Assess for depression, suicidal ideation
Since 2007, black-box warning in
patients

58
Q

Anxiety: associated with; SX

A

-Often associated with depression and psychiatric illness
-May be acute, transient, situational or chronic, persistent, and/or psychologic
Apprehension and reduced concentration
Fatigue and insomnia
Somatic (sympathomimetic)
Tachycardia, palpitations, and increased blood pressure (BP)
Hyperventilation, tremor, sweating, and GI issues

59
Q

Benzodiazepines: type of drug, action, how relieves anxiety

A

BZDs: sedative-hypnotics

  • Can result in: central nervous system (CNS) depression, decrease in activity, moderate excitement, depression of respiratory and vasomotor centers in CNS
  • Actions: sedation, hypnosis, decreased anxiety, muscle relaxation, anterograde amnesia (useful in surgery and procedures), anticonvulsant activity
  • Relief of anxiety primarily related to CNS depression (causing sedation, depressing respiratory and vasomotors centers in CNS)
60
Q

Benzodiazepines: indications and warning

A
  • Indications: for acute and short-term use in treatment of panic attacks, generalized anxiety disorder (GAD), insomnia, and EtOH (ethanol) withdrawal
  • BZDs can also be abused in date rape flunitrazepam Rohypnol)
61
Q

Types of Benzodiazepines: short, intermediate, and long-acting

A

-Short acting: no accumulation, less daytime sedation with nighttime dose, increased anterograde amnesia. Increased frequency of dosing, rebound insomnia, interdose rebound.
Ativan (lorazepam), Xanax (alprazolam), Serax (oxazepam)
-Intermediate acting: Valium (diazepam)
-Long acting: less frequent dosing, no interdose rebound, less severe withdrawal. Risk of accumulation and of next-day sedation.
Klonopin (clonazepam), Librium (chlordiazepoxide)
High potency: short acting and more withdrawal symptoms
Low potency: increased duration, more rapid onset of action, and more abuse risk

62
Q

Pharmacodynamics of Benzos:

A
  • Bind to molecular components of the gamma-aminobutyric acid (GABAA) receptors in the neuronal membranes in the CNS
  • GABAA is an amino acid and a major inhibitory neurotransmitter
  • GABAA receptor is an integral membrane chloride channel and mediates most of the rapid, neuroinhibitory transmission in the CNS
  • Potentiate GABA-ergic inhibition at all levels of the CNS leads to decreased firing rate of critical neurons in many regions of the brain
  • BZDs increase the amount of chloride current generated by GABAA receptor activation, potentiating the effects of GABA throughout the nervous system
63
Q

Benzos: Distribution, Metabolism, Excretion

A

-Distribution: all have high lipid solubility, protein binding is not clinically significant: 0–98%
-Metabolism: classified according to half-life, which depends on rate of metabolic transformation
-Extensive hepatic metabolism
Phase I (3A4, 2C19) and II (glucuronidation)
Active metabolites
-Excretion: renal
Most BZDs are completely absorbed and rapidly distributed to CNS. There is redistribution of drug from tissues to plasma (prolonged elimination).

64
Q

Benzos: adverse effects

A
  • Excessive sedation: dizziness, lethargy, and ataxia
  • Respiratory depression: can be fatal in OD, but usually only in a patient with underlying pulmonary dysfunction or in combination with other CNS/respiratory depressants (EtOH)
65
Q

Benzos: tolerance, cross-tolerance, and dependence; withdrawal SX

A

Tolerance: decreased responsiveness to the drug following repeated exposure
Cross tolerance occurs with alcohol
Physiologic dependence: altered physical state that requires continuous drug administration to prevent withdrawal symptoms. May include increased anxiety, insomnia, CNS excitability that can progress to convulsions. Severity of withdrawal symptoms depends on individual drugs and size of dose.
Half-life also affects withdrawal. Longer half-life results in self-tapering.

66
Q

Benzos: elderly and pregnancy use?

A
  • Caution elders

- Pregnancy Category C or D

67
Q

Pt Monitoring and education:

A 
-Monitor for side effects
Excessive sedation
-Monitor for escalating use
Patient education
-Do not use alcohol or other CNS depressants (kava-kava).
-Do not increase prescribed doses.
-Slowly taper the drug after prolonged use.
-Use caution with driving.
68
Q

Reversal of Benzos:

A

-The only BZD antagonist available for clinical use currently blocks many of the actions of BZDs but does not antagonize CNS effects of other sedative hypnotics, opioids, ethanol, or general anesthetics.
Antagonist
Flumazenil (Romazicon)
Parenteral: 0.1 mg/ml IV
-Antagonism of BZD-induced respiratory depression is less predictable.
-All BZDs have a longer half-life than flumazenil (0.7–1.3 hours) and require several doses.
-Adverse effects: agitation, dizziness, nausea, severe abstinence syndrome in dependent patients
-Seizures and cardiac arrhythmias in patients who have ingested BZDs with tricyclics

69
Q

Insomnia: RX options

A 
-Hypnotic, nonbenzodiazepine
Zolpidem (Ambien)
Eszopicione (Lunesta)
-Serotonin receptor antagonists
Trazedone, Remeron
-Tricyclics
Elavil
70
Q

Diagosing ADHD: general guidelines

A
  • Must be present for more than 6 months and in more than one setting
  • Needs to have been present before 12 years of age
  • Requires obvious difficulty with job, school, or social setting
  • Changes in DSM-5 criteria allows for autistic patients to be diagnosed with ADHD
71
Q

ADHD DX: 3 components

A

Inattention, Hyperactivity, Impulsivity,

72
Q

Pathogenesis of ADHD:

A
  • Genetics
  • Pre- and postnatal factors (e.g., cigarette smoking)
  • Environmental factors
  • Changes in the brain: shows in frontal, parietal, and temporal lobes
  • Abnormal dopamine uptake
  • Abnormal norepinephrine production
73
Q

ADHD TX is a combo of:

A

Combination of

  • Environmental modification (school, work)
  • Behavioral modification
  • Medication
74
Q

ADHD Meds: 1st line; other FDA-approved; non-FDA approved

A 
Medication
-First line: long-acting medications
Stimulants
Nonstimulants
-Other FDA-approved medications
Clonidine
Guanfacine
-Non-FDA-approved medications (due to side effects)
Modafinil
Bupropion
75
Q

Consequences of not treating ADHD:

A

Consequences are well documented in the literature.

  • Poor school success
  • Difficulty with friendships
  • Increased conflict with parents
  • Increased risk-taking behaviors
  • Increased rates of substance abuse
  • Increased injuries
  • Increased motor vehicle accidents
76
Q

How to DX ADHD (ie scales, DSM)

A

-DSM criteria need to be met
-For children, the parent and teacher need to complete a validated tool for diagnosis
Conners scale
Vanderbilt scale
Others
-For adults
Conners adult scale
Brown attention deficit disorder scale
Others

77
Q

Stimulants in ADHD

A
  • Start with a low dose and then slowly titrate up until symptoms are controlled with minimal side effects
  • Choose between short-acting and long-acting medications
  • Use alternative forms of medication for people that cannot swallow pills
78
Q

Preferred meds in ADHD

A

-Preferred medications for ADHD are mixed amphetamine salts and methylphenidate (stimulants) due to best safety profile and effect

79
Q

Types of Stimulants in ADHD:

A
  • Mixed amphetamine salts: Adderall and Adderall XR
  • Methylphenidate: Concerta, Methylin, Daytrana, Ritalin, Ritalin SR, Ritalin LA, and Metadate
  • Dextroamphetamine: Dexedrine and Dexedrine Spansules
  • Lisdexamfetamine: Vyvanse
  • Dexmethylphenidate: Focalin and Focalin SR
  • Dexamfetamine sulfate: Dexamed (Kohne Pharma) is approved in Europe and is the cousin to Adderall XR
80
Q

RX ADHD meds with cardiac/ tic disorders

A
  • For all children who are to initiate medication for ADHD, perform a careful cardiac history and physical:
  • Personal history of cardiac symptoms
  • Family history of cardiac problems, especially arrhythmias, sudden death, or death at a young age from a cardiac cause
  • Vital signs
  • Cardiac physical exam
  • *Obtain an EKG if there is any history of chest pain, palpitations, syncope, or shortness of breath during exercise.
  • *For children with tic disorders, manage carefully or see them in collaboration with a specialist if you need to prescribe a stimulant.
81
Q

Contrindications to Stimulant RX:

A
  • History of schizophrenia or other psychosis
  • Prominent symptoms of anxiety, tension, and agitation
  • History of drug abuse by the patient, family, or friends
82
Q

Short-acting vs. long-acting stimulants:

A

-Short-acting medications
Typical dosing in the past: two short-acting tablets, one in the morning and one at lunch
Still in use (fewer night time symptoms)
-Long-acting medications
More expensive
Have the benefit of only dosing once daily
Eliminate any stigmatization of taking a pill at lunch
**Both can be used in conjunction as long as the maximum daily dose is not exceeded.

83
Q

Methylphenidate: preparations

A 
-Short acting
Methylin or Ritalin
Initiate at 5 mg (max dose 60 mg/day)
Duration of 3–5 hours
-Long acting
Concerta
18–72 mg/day
Duration of 12 hours
Methyl ER
10–60 mg
Duration of 8 hours
Ritalin LA
20–60 mg
Duration of 6–8 hours
Metadate CD
20–60 mg
Duration of 6–8 hours
Daytrana (patch form)
10–30 mg, wear for 9 hours
Duration of 11–12 hours
84
Q

Other major stimulants:

A

-Mixed amphetamine salts
Adderall SA: 2.5–40 mg; duration 6 hours
Adderall XR: 5–40 mg; duration 10 hours
-Dextroamphetamine
Dexedrine/Dextrostat: 3.5–40 mg; duration 4–6 hours
Dexedrine Spansules: 5–40 mg; duration ≥6 hours
**Not preferred due to increased side effect panel and risk of addiction
-Lisdexamfetamine
Vyvanse: 2–70 mg/day; duration 10–12 hours
Prodrug of dextroamphetamine
Lysine bound to dexamfetamine, cleaved in intestine to activate
**Lower abuse potential due to activation method
-Dexmethylphenidate
Focalin: 2.5–20 mg; duration 3–5 hours
Focalin XR: 5–30 mg/day; duration 8–12 hours
Enantiomer of methylphenidate

85
Q

Common SEs for stimulants

A
  • Delay in sleep onset
  • Anorexia and suppressed appetite
  • Worsening of tics (uncertain)
  • Headaches
  • Abdominal pain
  • Increased blood pressure
  • Skin irritation (with Daytrana)
86
Q

Rare SEs of stimulants

A
  • Growth deceleration
  • Blood dyscrasias
  • Fearfulness
  • Depressive episodes
  • Hallucinations and confusion
  • Problems with seizures
  • Rebound effect (with short-acting medications)
  • Priapism
87
Q

Clinical pointers: stimulants

A
  • It is preferred to try three different stimulants prior to trying a nonstimulant medication.
  • Children and adolescents may require higher doses of stimulants than adults because of their higher metabolism.
  • Start low and increase the dose each week, monitoring closely for effectiveness and side effects.
  • Stimulants may bring out underlying psychosis.
88
Q

NONstimulant ADHD meds: Strattera

A

=Noradrenergic reuptake inhibitor
First nonstimulant to be approved by the FDA for ADHD treatment
Dosing
0.5 mg/kg/day to initiate, titrate up to 1.2 mg/kg/day
Max dose is 100 mg/day or 1.4 mg/kg/day
Can dose BID if 24-hour coverage is needed
**No immediate effect: can take weeks, like antidepressants

89
Q

Strattera: CAUTIONS

A
  • Metabolized by cytochrome P450: 2D6-interaction with fluoxetine, paroxetine, and quinidine
  • Contraindicated in narrow-angle glaucoma, within 2 weeks of an MAO inhibitor
  • Caution required with hypertension, tachycardia, cardiovascular, or cerebrovascular disease
  • Caution also required with concurrent albuterol use
  • **Black-box warning for possibility of suicidal ideation when initiating
  • Screen for thoughts about self-harm or increasing agitation
  • Can cause severe liver damage
90
Q

Strattera: Common SEs

A

Common side effects

  • GI discomfort and vomiting
  • Fatigue
  • Anorexia
  • Dizziness
  • Mood swings
  • Increase in blood pressure and heart rate
91
Q

Strattera: Rare SEs

A

Rare side effects

  • Hypersensitivity reactions
  • Agitation
  • Liver damage
  • Mania
92
Q

Non-stimulant in ADHD: Clonidine

A

=alpha-2 agonist
-Effectively reduces aggression and hyperactivity
-May have some effects on tics as well
Usual dosing
Short-acting clonidine
0.05 mg qhs–0.4 mg/24 hours
Long-acting clonidine (Kapvay)
0.1–0.4 mg/24 hours
Duration of 10–12 hours
**Should not be discontinued abruptly: always taper
**Rebound hypertension can occur with abrupt withdrawal
*Lost favor due to “slowing” effect in children (slowed too much)
*Back in favor in ER form

93
Q

Clonidine: SEs

A
  • Hypotension
  • Dry mouth
  • Dizziness
  • Drowsiness and fatigue
  • Constipation
  • Anorexia
  • Arrhythmias
  • Depression
94
Q

NON-stimulant in ADHD: Guanfacine

A 
=alpha-2 agonist
Short-acting version: Tenex
0.5–4 mg/day in divided doses
Long-acting version: Intuniv
0.1–0.4 mg/day (QD–BID)
Duration of 10–12 hours
* Less sedating than clonidine
* Being used a lot more recently!
95
Q

Guanfacine SEs

A
  • Drowsiness
  • Dizziness
  • Insomnia
  • GI issues
  • Hypotension
  • Fainting
96
Q

Non-FDA approved alternative meds in ADHD: Modafinil

A
  • Used for hypersomnia in adults
  • Common side effects: headache, insomnia, and anorexia
  • During testing: showed improved ADHD scores, but weight loss was common
  • Also associated with Stevens–Johnson rash
97
Q

Non-FDA approved alternative meds in ADHD: Buproprion

A

-Noradrenergic effect
-Benefits with ADHD (from adult data)
Dosage
Starting at 75 mg/day
Given BID, typically 75–300 mg/day
Available forms
Tablets of 75 mg and 100 mg
Sustained release (SR) tablets of 100 mg, 150 mg, and 200 mg
Extended release (XL) tablets of 150 mg and 300 mg
-Side effects
Similar to those for clonidine
Activation can occur
-Seizures are rare (0.4%) and are even less likely with SR and XL forms
-Anorexia, agitation, depression, or self-injury

98
Q

Pt monitoring in ADHD

A
  • While at the discretion of the prescriber, once every 1–3 months is usual
  • Include blood pressure, weight, heart rate, and side effect review
  • Assess target goals
  • Adjust the medication as needed
  • Collaborate/refer if needed
  • Maintain contact with school
99
Q

Higher risk for abusing ADHD drugs:

A

Higher risk if

  • Caucasian
  • Member of a fraternity or sorority
  • GPA is low
  • Medication taken is immediate release
  • Multiple ADHD symptoms
100
Q

How to avoid misuse/ abuse of stimulants:

A
  • Screen all families and patients for substance use/abuse
  • Prescribe extended release stimulants: Vyvanse (popular)
  • Alternatively, use nonstimulant medications
  • Follow patients and your prescriptions carefully
101
Q

TICS and ADHD

A

-20% concurrence of ADHD and tic disorders
-50% of patients with Tourette’s will have ADHD
In the past, stimulants contraindicated in patients with tic disorders (biochemical relationship)
Not supported by evidence!

102
Q

If your patient with ADHD develops tics:

A

If your patient with ADHD develops tics

1) Stop the stimulant, with a retrial in a few weeks: monitor symptoms
2) If tolerates a short-acting stimulant, change to long acting
3) Change the stimulant
4) If that fails, change to a nonstimulant (e.g., atomoxetine)
5) Or use a stimulant combined with an Alpha-2 agonist
6) Rarely, an atypical antipsychotic is prescribed

103
Q

Complicating conditions with ADHD

A

For all patients
-Screen for depression, anxiety, psychosis, and aggression first
-Multimodal therapy will likely be needed
For anxiety disorders
-Strattera is better
-Stimulant, with SSRI for anxiety

Pharmacology (17 decks)

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