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Therapeutics 4 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Behavior depends on

A

Perception, Genetics, Experience

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2
Q

Biopsychosocial model

A

Biology, psychology, social, and environmental factors may ALL be important

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3
Q

Interventions for mental illness

A

Non-pharm neuromodulation, pharmacological interventions, psychotherapy and illness education

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4
Q

Neuroplasticity

A

Allows an individual to adapt to a rapidly changing environment through strengthening, weakening, pruning, or adding of synaptic connections and by promoting neurogenesis.

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5
Q

Neuroplasticity in daily life

A

Long term potentiation (LTP)- strengthens neuronal connections.
Long term depression (LTD)- weakens neuronal connections.
Global processing- forms big picture understanding, context.
Local processing- perceives small details, faces

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6
Q

Factors of change in neuroplasticity

A

Age

Illnesses

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7
Q

Types of brain damage

A 
Tumors/malignancies
Strokes
TBI
Infections/toxins
Congenital disease
Epilepsy
Neurodegenerative conditions- dementia, huntingtons, parkinsons
Mental illness
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8
Q

Common neurotransmitters in mental illness

A

BDNF, Glutatmate, GABA, acetylcholine, DA, serotonin, NE

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9
Q

BDNF

A

Promotes neurogenesis

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10
Q

Glutamate

A

Neuronal development, synapse organizations, DA regulation

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11
Q

GABA

A

Neuronal circuitry in prefrontal cortex, inhibition

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12
Q

Acetycholine

A

Cortical plasticity, processing senses

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13
Q

DA

A

Reward, positive symptoms

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14
Q

Serotonin

A

Multiple functions,modulates BDNF

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15
Q

NE

A

Arousal, sensory integration, memory

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16
Q

Illness education

A

Stigma- taking the vagueness out of mental illness, making it medical.
Expectations- time needed for neurons to grow or change. May not feel better with one dose/session.
Balancing interventions- behavior/environment, meds, both have neuronal impact

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17
Q

Psychotherapy examples

A

Cognitive behavioral therapy
Dialectical behavioral therapy
Exposure therapy
Eye movement desensitization and reprocessing

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18
Q

Who is most likely to benefit from psychotherapy?

A

Depression, anxiety, PTSD, OCD
May be effective in bipolar, ADHD
Minimal benefit in schizophrenia

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19
Q

Bright light therapy

A

Bright light intended to mimic sun exposure
Controlled exposure of intense, but safe light
-6,000-10,000 lumens for 30 min/day
UV filtered

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20
Q

Bright light therapy risk vs benefit

A

Risk- choosing a good product, photosensitive agents, AE

Benefits- may help sleep disorders, safe, patient accepted.

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21
Q

Who is most likely to benefit from bright light?

A

Depression= first line in SAD

Bipolar disorder if absence of mania, must be on an anti-manic

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22
Q

Repetitive transcranial magnetic stimulation

A

Brain stimulation therapy
Electromagnetic coil is placed against the head in a specific location and short pulses pass through the skull and stimulate nerve cells. Treatments lasts 4-6 wks and is 5 days/week

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23
Q

Risks vs benefit of rTMS

A

Risks- very expensive, contraindications similar to MRIs, timely, AE
Benefits- less AE than ECT, well accepted if the patient has time and money, noninvasive

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24
Q

Who is likely to benefit from rTMS?

A

Depression= 2nd or 3rd line

Bipolar- 3rd line

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25
Q

Electroconvulsive therapy (ECT)

A

A procedure given with neuromuscular blockers and generalized anesthesia (sedated then paralyzed then electrical current then seizure then recovery)
Can be done outpatient.

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26
Q

Process of ECT

A

Psychiatric and medical examination- informed consent- 3 treatments/week for 2-4 weeks, f/u

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27
Q

ECT risk vs benefit

A

Risk= AE

Benefit- high efficacy rate, faster than antidepressants. Safe in pregnancy, elderly, very low mortality rates

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28
Q

Who is most likely to benefit from ECT?

A

Depression- 1st line in severe/psychosis
Bipolar- 2nd line in bipolar depression
Some evidence in schizophrenia

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29
Q

Sedative

A

A drug that produces a calming state and reduction of anxiety

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30
Q

Hypnotic

A

A drug that produces drowsiness, facilitates sleep

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31
Q

Anxiolytic

A

A drug that reduces anxiety

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32
Q

Barbiturates

A

Classified based on duration of action
Tolerance- greater to sedation than to anticonvulsant or lethal effects; thus narrow therapeutic index
Thiopenal, methohexital, pentobarbital, secobarbital, amobarbital, phenobarbital

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33
Q

Which barbiturates are ultrashort acting (5-15 minutes)

A

Thiopental, methohexital, pentobarbital

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34
Q

Which barbiturates are short acting (3-8 hours)?

A

Pentobarbital, secobarbital, amobarbital

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35
Q

Which barbiturate is long acting (days)

A

Phenobarbital

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36
Q

Benzodiazepines

A

Term refers to portion of chemical structure composed of benzene ring; halogens (F, Cl) increase lipid solubility.
Broad spectrum of activity- anxiolytics, sedatives, hypnotics, muscle relaxants, anti-convulsants

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37
Q

Advantages of benzodiazepines

A

High margin of safety, little respiratory or CV depression

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38
Q

Which therapeutic uses of benzodiazepines require a long 1/2 life?

A

Anticonvulsant, anxiolytic

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38
Q

Which therapeutic uses of benzodiazepines require a long 1/2 life?

A

Anticonvulsant, anxiolytic

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39
Q

Which therapeutic uses of benzodiazepines requires rapid entry into the brain?

A

Status epilepticus

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40
Q

Which therapeutic use of benzodiazepines requires short elimination 1/2 life

A

Hypnotic

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41
Q

Short acting benzodiazepines

A

Midazolam, triazolam

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42
Q

Intermediate acting benzodiazepines

A

alprazolam, clonazepam, oxazepam, temazepam

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43
Q

Long acting benzodiazepines

A

Chlordiazepoxide, diazepam, flurazepam

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44
Q

GABA/Benzodiazepine receptor complex

A

All clinically important actions are mediated by the GABA-benzodiazepine receptor complex.
Ion channel that facilitates chloride entry into neuron leading to hyperpolarization and reduced neuronal firing.

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45
Q

GABA-Benzo receptor ligands

A

GABA, Benzo,

Benzo antagonist- flumazenil

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46
Q

What drug is used for Benzo OD

A

Flumazenil

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47
Q

Benzo AE

A

CNS depression: sedation, psychomotor impairment, ataxia, abuse
Anterograde amnesia
Physical dependence/withdrawal
Interactions with alcohol and other sedatives.

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48
Q

Buspirone

A

Non-benzo anxiolytic.
Agonist at 5-HT1A receptors. Does not exhibit cross tolerance with benzos
Anxioselective- has no other properties

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49
Q

Buspirone advantages and disadvantages

A

Advantage- fewer and less severe CNS effects compared to benzos (no physical dependence)
Disadvantage- slower OOA, 1-2 weeks

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50
Q

Benzo vs. buspirone

Relief of generalized anxiety

A

Both

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51
Q

Benzo vs buspirone

Which has addiction liability

A

Benzo

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52
Q

Benzo vs buspirone, which has rebound anxiety?

A

Benzo

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53
Q

Benzo vs buspirone, which has physical dependence?

A

Benzo

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54
Q

Benzo vs buspirone, which has delay in anxiolytic effect?

A

Buspirone

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55
Q

Benzo vs buspirone, which potentiates alcohol sedation

A

Benzo

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56
Q

Hypnotics: Novel benzodiazepine agonists

A

Zolpidem, Zaleplon, Eszoplicone

Non-benzo that act as agonists or positive allosteric modulators at the GABA/Benzo receptor complex

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57
Q

Novel benzo agonists BBW

A

Risk of serious injuries in sleepwalking

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58
Q

Novel benzo agonists (z drugs) properties

A 
Strong sedative effects mask anxiolytic  action
Only weak anticonvulsant effect
Little evidence of physical dependence
Short 1/2 life
No rebound insomnia
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59
Q

Novel benzo agonists (z drugs) MOA

A

Binds to alpha-1 subunit containing sites

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60
Q

Hypnotics: melatonin receptor agonists

A

Ramelteon and Tasimelteon
Activates melatonin receptors
Rapid onset with minimal rebound insomnia

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61
Q

Suvorexant

A

Orexin antagonist
Lacks abuse potential
Hypnotic but not sedating

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62
Q

Drugs for bipolar disorder

A

Lithium

Carbamazepine, valproate, lamotrigine, quetiapine, cariprazine

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63
Q

Etiology of depression

A

Biogenic amine hypothesis
-Disorders of mood result from dysfunction of brain monoamine neurotransmitters (serotonin and NE primarily)
Newer focus on neuroplasticity

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64
Q

What type of diet promotes depression?

A

Tryptophan deficient diet

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65
Q

Classification of antidepressants

A

Tricyclic antidepressants (TCAs)
Selective serotonin (5-HT) reuptake inhibitors (SSRIs)
Selective serotonin-NE reuptake inhibitors (SNRIs)
Monoamine oxidase inhibitors (MAOIs)
Heterocyclics
Ketamine

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66
Q

TCA drugs

A

Amitriptyline, desipramine, imipramine

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67
Q

TCA MOA

A

Inhibit the reuptake mechanisms (transporters) responsible for the termination of the synaptic actions of both NE and 5-HT in the brain. Results in potentiation of their neurotransmitter actions at postsynaptic receptors

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68
Q

TCA effects

A

Acute- block the reuptake of NE and 5-HT.

Delayed- Weeks, therapeutic onset with all antidepressants (except ketamine)

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69
Q

Tricyclic antidepressants AE

A

Muscarinic ACh blockade- dry mouth, urinary retention, constipation
a-adrenergic (NE) blockade- orthostatic hypotension
Histamine blockade- sedation, weight gain
Sodium channel blockade- cardiac toxicity

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70
Q

Selective serotonin reuptake inhibitor agents

A

Fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, escitalopram

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71
Q

SSRIs acute effects

A

Selectively block reuptake of 5-HT. Minimal inhibitory effect on NE transporter or blockade of ACh or NE receptors

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72
Q

What is better tolerated, SSRIs or TCAs?

A

SSRIs

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73
Q

Serotonin-norepinephrine reuptake inhibitors (SNRIs) MOA

A

SNRIs bind and inhibit transporters for both NE and 5-HT

Enhance the actions of both neurotransmitters

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74
Q

SNRIs drugs

A

Desvenlafaxine, duloxetine, venlafaxine, levomilnacipramine

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75
Q

How do SNRIs differ from TCAs?

A

In lacking significant blocking effects on peripheral receptors including H1, muscarinic, or a-adrenergic receptors

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76
Q

Serotonin receptor antagonists/ SRI agents

A

Trazodone, nefazodone (not us)

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77
Q

Serotonin receptor antagonists actions

A

5-HT2A/C receptor antagonist and 5-HT uptake inhibitor

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78
Q

Vilazodone

A

Antidepressant

5-HT reuptake inhibitor/ 5-HT1a partial agonist`

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79
Q

Vortioxetine

A

Antidepressant

5-HT stimulator/modulator

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80
Q

Monoamine oxidase inhibitors drugs

A

Phenelzine and tranylcypromine
Non selective inhibitors of MAO A and B, inhibit NE and 5-HT
Selegiline- selective inhibitor of MAO-B at low doses

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81
Q

MOA of MAOIs

A

Inhibit monoamine oxidases that metabolize NE and 50HT and dopamine
Increase vesicular stores of 5-HT and NE

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82
Q

DDI and MAOIs

A

Foods containing tyramine with MAOIs can lead to htn crissi

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83
Q

Which antidepressants have the worst sexual AE

A

SSRIs
Venlafaxine
Some- tricyclics, MAOIs

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84
Q

Which antidepressants have the worse conduction AE

A

Tricyclics

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85
Q

Which antidepressants have the worst seizure AE

A

Bupropion is worst
Tricyclics
Some- venlafaxine, SSRIs, trazadone

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86
Q

Which antidepressants have the worst sedation?

A

Tricyclics, trazodone

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87
Q

Which antidepressants have the worst anti-adrenergic (orthostatic hypotension) AE

A

Tricyclics

Trazodone

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88
Q

Which antidepressants have the worst anticholinergic AE

A

Tricyclics

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89
Q

Acute antidepressant drug action

A

Increased concentrations of transmitter in synapse, Predictive of antidepressant action.

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90
Q

Chronic antidepressant drug action

A

Enhanced 5-HT and NE transmission

Down regulation of receptors

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91
Q

Rapid acting antidepressant

A

Ketamine

-lack of sustained response

92
Q

Post-partum depression

A

Brexanolone

93
Q

Bipolar agents (mood stabilizers)

A

Prophylactic treatment

Lithium

94
Q

AE of lithium

A

Low therapeutic index
Polydipsia and polyuria
Renal toxicity
CNS AE is tremor

95
Q

Biopsychosocial model

A

Biology, psychology, social, and environmental factors may all be important in psych disorders

96
Q

Prevalence of MDD in US adults

A

Very common
Female
Native Americans
Low socioeconomic status
Stressors- medical, mental, socioeconomic
First-degree relative with depression (40-50% heritability)

97
Q

DSM-5 Diagnosis of MDD

A

Depressed mood and/or anhedonia (lack of pleasure) occurring almost every day for >2 weeks
AND
5+ additional symptoms that cause significant distress and/or impairment in social or occupational functioning

98
Q

Signs of depression (D-SIGECAPS)

A 
Depressed mood
Sleep- insomnia or hypersomnia
Interest- diminished 
Guilt- feelings of worthlessness 
Energy- loss
Concentration- diminished
Appetite- significant weight loss or gain
Psychomotor agitation or retardation
Suicide
99
Q

Standardized rating scales for MDD

A 
HAM-D
MADRS
PHQ-9
PHQ-2
QIDS
100
Q

MDD differential diagnosis

A

Rule out non-organic causes

  • substance use (alcohol, benzodiazepines)
  • Medications can cause “depression-like” symptoms
  • Other medical conditions- hypothyroidism, anemia, heart disease
101
Q

Drug induced depression

A

Antihypertensives- Beta blockers, calcium channel blockers
CNS depressants- alcohol, benzodiazepines, opioids
Anti-infectives- fluoroquinolones, acyclovir
Misc. - Isotretinoin, oral contraceptives, corticosteroids

102
Q

Response and remission of depression

A

Untreated episodes usually last around 6 months
Periods of remission shorten with subsequent episodes
1/2 will fully respond
15% may never experience remission/recovery

103
Q

Depression recurrence

A

About 1/2 of patients will experience a single episode
Patients who have experienced 3 or more episodes exhibit a 90% recurrence.
Other risk factors-chronic medical conditions, other psychiatric comorbidities, childhood maltreatment

104
Q

Depression and suicidality

A

If untreated, lifetime risk of suicide is about 20%
Highest in older (>75 yo) white males, LGBTQ+, teenager/ adolescents
Other risk factors: IS PATH WARM

105
Q

IS PATH WARM suicide risks

A 
ideation 
substance abuse
Purposelessness
anxiety
Trapped
Hopelessness
Withdrawal
Anger
Recklessness
Mood change
106
Q

Pathophysiology of depression

A

Monoamine deficiency
Receptor dysregulation
Chronic stress
Unknown

107
Q

Monoamine hypothesis of depression

A

Based on the MOA of the earliest antidepressants.
MAOIs and TCAs work to increase the levels of NE, Serotonin, and Dopamine
Hypothesis: Depressed patients are deficient in monoamine neurotransmitters
….but antidepressants increase neurotransmitters in the synapse on day 1 and antidepressants dont work for weeks.

108
Q

Neurotransmitter receptor hypothesis (AKA sensitivity hypothesis) of depression

A

Extension of monoamine hypothesis
Attempts to account for delayed antidepressant activity
Hypothesis: Depletion of monoamine neurotransmitters leads to neural hypersensitivity and receptor up-regulation.
…but there is no reproducible evidence of consistent monoamine deficiency in depressed patients

109
Q

Monoamine hypothesis of gene expression (stress model) of depression

A

Evidence that despite normal monoamine levels and their receptors, these systems do not respond normally in depressed patients.
Cortisol is released causing a reduction in brain-derived neurotrophic factor (BDNF)
Hypothesis: Serotonin enhances BDNF and neurogenesis in the hippocampus, reversing negative effects of cortisol. Glutamate modulation quickly releases BDNF in the brain.

110
Q

Summary of theories of depression

A

There appears to be a dysfunction in the frontal cortex and limbic structures
Manipulation of serotonin and NE systems can alter depressive symptoms

111
Q

MDD: Treatment algorithm

A

1st line- SSRI (except fluvoxamine), SNRI, NaSSA, NDRI, vortioxetine
Titrate for 1-4 weeks
No response- change agent, test for weeks 4-8
Partial response- augment, increase dose, change agent, psychotherapy
Full response- continue for 4-9 months or indefinite
3rd line- TCAs, MAOIs, misc, augmenting agents

112
Q

St. Johns Wort

A 
Modest efficacy
TID
Induces multiple CYP enzymes
ADRs- N/V/D, photosensitivity, sexual dysfunction
Just put them on an SSRI instead
113
Q

A-adenosyl methionine (SAMe)

A

Low/modest efficacy in depression

ADRs include dizziness, dry mouth, constipation, insmonia

114
Q

L-methylfolate in depression

A

Prescribed medical food
Well tolerated, mixed efficacy
Adjunt in MTHFR polymorphism

115
Q

Omega 3 fatty acids in depression

A

Safe

Low efficacy

116
Q

Vitamin D in depression

A

Deficiency more common in depressed patients

Efficacy is mixed, does not prevent depression

117
Q

Classes of antidepressants

A 
SSRIs
SNRIs
NDRIs
NaSSa
ASRIs/SPARI
TCAs
MAOIs
Misc.
118
Q

STAR*D trial

A

The largest, longest duration controlled trials ever conducted to study depression.
Studied patients in multiple settings and in multiple phases of treatment.
Level one- start with citalopram and then add additional agents or switch if necessary

119
Q

BBW for all drugs approved for MDD

A

Increased risk of suicidality

120
Q

Serotonin syndrome

A

Applies to any agents with serotonergic properties
Potentially life threatening
Management- remove offending agent, 5-HT2A antagonists (cyproheptadine)

121
Q

Serotonin syndrome triad

A

Mental status changes, autonomic instability, neuromuscular abnormalities

122
Q

Serotonin syndrome s/s

A

Mental status changes- agitation, pressured speech
Autonomic instability- tachycardia, diarrhea, shivering, diaphoresis, mydriasis
Neuromuscular abnormalities- Clonus, hyperreflexia tremor, seizure

123
Q

Anti-depressant withdrawal

A 
Agents should be tapered over weeks if able (except fluoxetine, it self tapers)
Abrupt d/c can precipitate withdrawal syndrome
Flu-like symptoms
Insomnia
Nausea
Irritability
Sensory disturbance
HA
(FINISH)
124
Q

Serotonin selective reuptake inhibitors (SSRI) MOA

A

Inhibition of reuptake of serotonin in the presynaptic neuron of the CNS.

125
Q

When to use SSRIs

A

1st line agent for MDD

Low risk of toxicity in overdose

126
Q

SSRIs agents

A 
Fluvoxamine
Fluoxetine
Paroxetine
Escitalopram
Citalopram
Sertraline
127
Q

Citalopram dosing

A

10-40mg QD

*max 20mg if >60 years old, significant hepatic impairment, and 2C19 PM

128
Q

Which SSRI has the longest T1/2?

A

Fluoxetine
4-6 days T1/2
Metabolite in 4-16 days

129
Q

SSRIs: sexual dysfunction

A

Very common, about 1/3 of patients
Decreased libido, delayed ejaculation, anorgasmia
Treatment strategies- wait before changing therapy as tolerance may develop, use sildenafil for erectile problems, add bupropion, mirtazapine, buspirone

130
Q

Which SSRI causes sexual dysfunction most commonly?

A

Paroxetine

131
Q

SSRIs AE

A 
N/V/D
Insomnia
Fatigue/sedation
Weight gain
Diaphoresis
Seizures
SIADH (rare)
Anxiety/agitation in early treatment
Risk of bleeding- increased with other antiplatelet therapy added
132
Q

Which SSRI causes insomnia the most?

A

Fluoxetine

133
Q

Which SSRI causes N/V/D the most?

A

Sertraline

134
Q

Which SSRI causes fatigue the most

A

Paroxetine

135
Q

Which SSRI causes weight gain the most?

A

Paroxetine

136
Q

Paroxetine-specific SSRI AE

A

Anticholinergic effects (avoid in elderly)

137
Q

Citalopram-specific SSRI effect

A

QTc prolongation

Do not give more than >40mg/day or 20mg if >60 years old

138
Q

SSRIs DDI

A

All SSRIs:
MAOIs- hypertensive crisis, serotonin syndrome. Linezolid also has MAOI effects.
Triptans, sibutramine- serotonin syndrome
NSAIDs, antiplatelets, anticoagulants- bleeding risk

Fluoxetine, paroxetine- Potent CYP2D6 inhibition, may increase conc of tricyclic antidepressants, may interfere with tamoxifen treatment

Fluvoxamine- CYP1A2 potent inhibition

139
Q

Serotonin/NE Reuptake Inhibitors (SNRIa) MOA

A

Inhibit both serotonin and NE presynaptic reuptake
More specific to NE-5HT than TCAs (better safety and tolerability)
1st line

140
Q

SNRI agents

A

Levomilnacipran
Duloxetine
Venlafaxine
Desvenlafaxine

141
Q

SNRIs AE

A

All:
N, dizziness, insomnia, sedation, constipation, sexual dysfunction, urinary retention, risk of SIADH
Dose related increase in diastolic BP

142
Q

Which SNRIs do you have to caution with uncontrolled narrow angle glaucoma?

A

Duloxetine, Levomilnacipran

143
Q

Which SNRI has the most pronounce increase in diastolic BP?

A

Venlafaxine and desvenlafaxine

144
Q

Which SNRI has risk of tachycardia?

A

Levomilnacipran

145
Q

Which SNRI has risk of rare interstitial lung disease?

A

Venlafaxine, desvenlafaxine

146
Q

Duloxetine-specific SNRI AE

A

More anticholinergic AE, urinary retention

Increases risk of hepatotoxicity, esp with ETOH

147
Q

SNRIs DDI

A

All-

serotonin syndrome, bleeding risk

148
Q

Duloxetine DDI

A

Substrate of CYP 1A2, 2D6

Inhibitor of 2D6

149
Q

Venlafaxine DDI

A

Substrate of 3A4, 2D6

150
Q

Levomilnacipran DDI

A

Substrate of 3A4`

151
Q

Norepinephrine dopamine reuptake inhibitor (NDRI) agent

A

Bupropion

152
Q

Bupropion MOA and use

A

1st line, augmenting agent
MOA: Inhibits reuptake transporters of synaptic dopamine, NE
Has NO serotonin effects

153
Q

Bupropion AE

A

N, V, weight loss, tremor, insomnia, xerostomia, HTN

Low risk of sexual dysfunction

154
Q

Bupropion DDI

A

MAOIs- HTN crisis
Seizure threshold lowering agents, beta lactam abx, alcohol, antipsychotics
CYP2B6 substrate, 2D6 inhibitor

155
Q

Bupropion contraindications

A

Seizure disorder
High alcohol/benzo intake
Bulimia, anorexia

156
Q

Noradrenergic and specific serotonergic antidepressant (NASSA) agent

A

Mirtazapine

157
Q

Mirtazapine MOA and use

A

1st line with compelling reason

MOA: antagonizes presynaptic a-2 adrenergic receptors (increase NE, serotonin) , H1 receptor antagonist

158
Q

Mirtazapine ADR

A

sedation, increased triglycerides, dry mouth, sexual dysfunction, appetite stimulation

159
Q

Vortioxetine MOA

A

1st line agent

SSRI with 5-HT1A agonism, mixed antagonist/partial agonist

160
Q

Vortioxetine AE

A

Nausea, constipation, vomiting, sexual dysfunction

161
Q

Vortioxetine DDI

A

CYP2D6 primary substrate- dose adjustment

Wait 21 days before starting MAOI (long t1/2)

162
Q

Serotonin antagonist/reuptake inhibitor (SARI) agents

A

trazodone, vilazodone

163
Q

Trazodone use and MOA

A

3rd line/ augmenting (d/t sedation)

MOA: Antagonist at post-synaptic 5HT2, inhibits reuptake of serotonin

164
Q

Trazodone AE

A

Sedation, dizziness, orthostatic hypotension

Priapism

165
Q

Trazodone DDI

A

Similar to SSRIs

Trazodone is 3A4 substrate

166
Q

Vilazodone use and MOA

A

MOA- SSRI and 5-HT receptor PARIAL agonist (SPARI)
Newer, less data
3rd line

167
Q

Vilazodone ADR

A

GI: Diarrhea, N, V, xerostomia
Neurologic: dizziness, insomnia
CYP3A4 substrate

168
Q

Tricyclic antidepressants use and MOA

A

3rd line for MDD
MOA: Inhibits reuptake of NE and 5-HT
Antagonizes histamine, alpha-adrenergic and muscarinic receptors, cardiac sodium channels (AE)

169
Q

Why has use fallen out of favor with TCAs?

A

OD can occur with a 1 week supply

Poor tolerability

170
Q

TCA agents

A 
Amitripyline
Imipramine
Doxepin
Clomipramine
Maprotiline
Protriptyline
Desipramine
Nortriptyline
171
Q

TCA AE

A 
Sedation
Decreased seizure threshold
CV events- orthostatic hypotension/syncope, arrhythmias
Sexual dysfunction
Tremor
Photosensitivity
Heat intolerance
Risk of seizure
172
Q

Anticholinergic effects of TCAs

A

Cholinergic rebound

Drying effects: SLUD

173
Q

Anti-histaminic effects of TCAs

A

Weight gain

Sedation

174
Q

Alpha-1 adrenergic effects of TCAs

A

Orthostasis
Hypotension
Dizziness

175
Q

TCA DDI

A 
CNS depressants
QT prolonging agents
alpha-adrenergic blockers (increases hypotension)
Serotonin syndrome
CYP interactions: 
2D6 substrates (except comipramine)
2C19 substrates (nortriptyline, doxepin)
1A2 substrate: clomipramine
176
Q

Monoamine oxidase inhibitors (MAOIs) moa and use

A

3rd+ line for MDD
MOA: Inhibition of MAOa and MAOb causing increased concentrations of NE, 5-HT, and dopamine in neuronal synapse
Infrequently used

177
Q

MAOI agents

A

Tranylcypromine
Isocarboxazid
Phenelzine
Selegiline

178
Q

MAOI AE

A 
Hypotension, dizziness common
Anticholinergic AE
Sedation or insomnia
HA
Sexual dysfunction
Cautions in cardiac disease, hepatic impairment
Contraindicated with pheochromocytoma
179
Q

MAOIs food interactions

A

Hypertensive crisis:
Food interaction from MAO-a inhibition in GI- excess of tyramine
Symptoms: stiff neck, HA, n, v, diaphoresis, increased BP
Dietary tyramine- cheese, wine, beer, fermented foods, MSG, coffee, chocolate
ALL MAOIs except selegiline patch

180
Q

MAOIs DDI

A

Serotonin syndrome- 2 week washout when changing to/from MAOI (5 weeks for fluoxetine, 3 weeks for vortioxetine)
Increased BP= stimulants, sympathomimetics *epinephrine, albuterol, decongestants

181
Q

MAO regeneration

A

14 days

182
Q

Esketamine

A

Intranasal jetamine
Used for augmentation in severe depression that has failed 2 trials of antidepressants
REMS program- must be administered by registered clinician and monitored for 2 hours after

183
Q

Antipsychotics in depression

A

FDA approved agents for augmentation- aripiprazole, brexpiprazole, olanzapine, quetiapine XR

184
Q

Additional depression augmenting agents

A

Stimulants

Buspirone

185
Q

Pharmacogenomics in depression

A

Polymorphisms in 2D6, 2C9, and 2C19 may affect medication levels
Short S or long L in 5-HT transporters, alterations in expression of BDNF and tryptophan hydroxylase may alter antidepressant response

186
Q

Depression in pregnancy

A

SSRIs most common (AVOID paroxetine)
SNRI
TCAs less frequently used, but has more data
Augmenting agents- mirtazapine, bupropion, antipsychotics

187
Q

AE of brexanolone

A

Presyncope, drowsiness, sedation, dizziness, xerostemia
BBW: Impairment/loss of consciousness
REMS required

188
Q

Depression drugs effects on lactation

A

Risk of AE from breastfeeding low
Some cases of somnolence with citalopram
Bupropion may decrease milk supply
“pump and dump” not recommended

189
Q

Pediatrics and adolescents depression agents

A

Start LOW and SLOW
recommend f/u in 1 week
Within 6 weeks change therapy if not effective

190
Q

Depression in elderly

A 
More physical symptoms- insomnia, pain
Less likely to respond to therapy
Low and slow
ECT is safe
SSRIs first line (avoid paroxetine, citalopram dose restriction)
Stimulants (methylphenidate) may help
191
Q

Which drugs are 1st line in depression?

A

SSRIs

192
Q

Is delirium reversible?

A

Yes

193
Q

Delirium

A

Disturbance of consciousness, attention, cognition, and perception.
Develops over a short period of time (hours to days)
Tends to fluctuate during the course of the day.

194
Q

DSM5 criteria for delirium

A

Alteration in attention and awareness
The alteration is abrupt and fluctuates throughout the day
There is also an alteration in cognition
Alterations are not better accounted for by any other disorder.
There is physical evidence that the alteration is caused by a medical condition, substance, or variety of causes

195
Q

Where is delirium found?

A 
Hospital
Long term care
ER
Palliative care 
Hospice
196
Q

How common is delirium in patients > 65 years old

A

50% of patients

197
Q

Where is delirium most common?

A

ICU

198
Q

Consequences of delirium

A

More than doubles mortality rate
Increases LOS by 2-5 days
1 in 3 patients have some residual cognitive impairment
Common cause of new institutionalization (delirium and incontinence most common causes)

199
Q

Confusion assessment method (CAM)

A

Must have acute fluctuation course and inattention

And disorganized thinking or LOC

200
Q

Delirium S/S

A 
Disturbed attention
Fragmented sleep
Memory impairment
Disoriented to time and place
Abrupt altered change in consciousness can be hyper or hypoactive
201
Q

Types of delirium

A

Hyperactive
Hypoactive
Mixed

202
Q

Symptoms of hyperactive delirium

A

Restlessness, agitation, hallucinations, delusions

203
Q

Which type of delirium is most common in the elderly?

A

Hypoactive or mixed.

Often unrecognized

204
Q

S/S of hypoactive delirium

A

Lethargy, sedation, slow response and movement

205
Q

Dementia vs delirium

A

Dementia- insidious onset, gradual deterioration
Awareness is often clear until advanced stages in dementia
Dementia pts do not have hallucinations or delusions until late stage
Dementia patients have reversed sleep cycles.

206
Q

Depression vs delirium

A

Depression- onset takes a while to develop.
Patients have low mood, does not fluctuate.
Depression is chronic
ADL- compromised in patients with depression

207
Q

Sundowning

A

Dysfunction of circadian rhythm
Behaviors that occur in the evening- confusion, agitation, pacing/wandering, increased verbal activity
Management- proper sleep hygiene. trazodone, melatonin

208
Q

Risk factors for delirium

A 
H/O ETOH use
Age >70
Kidney or liver disease
Poly pharmacy (>6 meds)
Sensory impairment
Dementia, depression, underlying brain disease, previous delirium
209
Q

Pharmacology of drug induced delirium

A

Dopamine activation

Cholinergic inhibition

210
Q

What causes delirium?

A 
Dementia and drugs
Electrolytes/Eyes, ears other senses
Lungs, liver, kidney, brain, heart
Infection
Retention
Injury
Unfamiliar environment
Metabolic
Sleep
211
Q

What electrolytes cause delirium

A

Hyponatremia

Hypercalcemia

212
Q

Anticholinergic drugs and delirium

A

TCAs (amitriptyline)
Antihistamines
Incontinence agents- tolterodine, oxybutynin
Antipsychotics- olanzapine

Promethazine
Digoxin
Skeletal muscle relaxants
Paroxetine
benztropine
Cefepime, quinolones, imipenem, linezolid
213
Q

Psychotropics

A

Lunesta, belsomra, sonata, ambien
Benzos
Antidepressants

214
Q

Other medication causes of delirium

A 
Metoclopramide
Steroids
H2RAs
all antihypertensives and diuretics
Drug withdrwaawl
Antiarrhythmics
NSAIDs
215
Q

Opioids and delirium

A

Highest risk-codeine, tramadol

All others have risk

216
Q

Prevention of delirium

A

Ensure sensory aids
Encourage hydration, mobility, senses intact
Maintain sleep pattern
Avoid sedation, catheters, loud noices

217
Q

Management of delirium principles

A

Treat underlying cause
D/C any new medication added if no clear cause.
Non pharm management is critical.
Antipsychotics are DOC, but no drug is FDA approved for delirium

218
Q

Evaluation of delirium

A 
BMP, ammonia and calcium
CBC
Urinalysis
B12
TSH
Tox screen
Vital signs
O2 saturation
219
Q

Non pharm delirium tx

A

Family involvement, sitter, normalize sleep-wake cycle, sensory evaluation, music, remove catheters, mobilize pt, avoid restraints, hydration and nutrition

220
Q

Medication tx of delirium hyperactive

A

Haloperidol, olanzapine, quetiapine
BBW- 7 days or less
Use only when delirium puts patients at risk to themselves or others

221
Q

Haloperidol for delirium

A

First line, especially if severe
Low doses Q 4 H
QTc prolongation
More effective in pts halllucinatinf

222
Q

Olanzapine for delirium

A

More sedating than haloperidol, but less likely to cause EPS

223
Q

Quetiapine in delirium

A

More appropriate for mild delirium
More sedating than haloperidol
Safest in parkinsons disease

224
Q

Acetylcholinesterase inhibitors in delirium

A

Consider with patients who have dementia

225
Q

Benzos in delirium

A

Only use for alcohol withdrawal or parkinsons related delirium

226
Q

Valproic acid in delirium

A

Appropriate for patients with underlying behavioral manifestations of dementia.
Not for acute delirium

227
Q

SAR of benzodiazepines

A

Aromatic ring
Electronegative electron withdrawing group (Cl, F, nitro)
Phenyl group- increases activity
Carbonyl or H-bond acceptor (could also be NH)
Hydroxyl group= shorter duration of action

Therapeutics 4 (8 decks)

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